Samson Notes For PLAB

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Anatomy

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ANATOMY

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NPLAB ACADEMY LIMITED BOW BUSSINESS CENTRE BOW ROAD 153-159 EMAIL: [email protected] Contact Numbers: 02089800039 Mobile: 07940433068

EPIDEMIOLOGY AND ANATOMY LECTURE NOTES 2013.

BLOOD SUPLY OF THE UPPER LIMB

1. On the right side:

Aorta-----brachiocephalic truncus-----subclavian artery ---> Axillary artery ---> Brachial artery---> radial and ulnar artery---> which form the palmer arch-----> digital arteries NB: The brachiocephalis truncus gives branch to common carotid artery and the subclavin artery gives branch to vertebral artery

2. On the left side direct from the aorta branches off common carotid artery and subclavian artery.

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2. VENOUS SYSTEM A. Deep veins B. Superficial veins

DEEP VENOUS BLOOD FLOW Palmer metacarpal --->deep palmer veins---->Radial and ulnar veins-------Brachial vein------->Axillary vein---subclavian------->brachiocephalic

SUPERFICIAL VEINS

1. BASILIC VEIN 2. CEPHALIC VEIN Both of which drain into brachial vein -------> subclavian vein -----
brachiocephalic ------Superior vena cava

SPECIAL NERVES:

1. FACIAL NERVE

Innervates the muscles of expression and anterior 2/3 of taste and oral cavity.

Branches:

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1. Greater petrosal nerve : innervates the nasal glands, palates, lacrimal glands. Supplies the stapedius, chorda tympani ( submandibular gland, sublingual gland and taste of the tongue. 2. Posterior auricular nerve: muscles around the ear 3. Temporal branch of facial nerve: 4. Zygomatic branch of facial nerve 5. Marginal branch of mental nerve 6. of facial nerve 7. Cervical branch of facial nerve

2. TRIGEMINAL NERVE

A. OPTHALMIC BRANCH comes out through superior orbital fissure. -Frontal nerve: Innervates the scalp, forehead, upper eye lid, conjunctiva and cornea -Nose (including the tip f the nose) -Frontal sinuses

B. MAXILLARY BRANCH-comes out from the skull through foramen rotundum

- Infraorbital nerve -Innervetes the cheek, upper lip, upper teeth and gums. -nasal mucosa, palate and roof of the pharynx -the maxillary, ethmoid and sphenoid sinuses and part of the meningitis

C. MANDIBULAR BRANCH -Comes out from foramen foramen ovale -Innervetes the lower lip, lower teeth and gums. -chin and jaw(but not the angle of jaw which is supplied by the C2-C3) -

Branches: i)

Lingual nerve

supplies the sensation of the anterior 23 of the tongue

-Inferior alveolar nerve supplies

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ii) Auriculotemporal nerve=is commonly gets injured during the tempomandibular surgery leading to loss of sensation on the auricule and skin surrounding ear

iii) Buccal nerve=supplies the mucus membranes of the buccal i. e inside

iv) Mental nerve: supplies the chin and lower lip (mucus membrane) it is the branch of inferior alveolar which itself is branch of mandibular branch of trigeminal.

Specific nerve damage:

1. T4 is level of nipples 2. T10 is umbilicus 3. C4 over acromioclavicular joint 4. Diaphragmatic nerve usually irritated in peritonitis causing shoulder tip pain. Also known as phrenic nerve. 5. Claw hand is a sign if ulnar nerve damage. Usually the little finger and ring finger are affected 6. Wrist drop is a sign of radial nerve damage. 7. Carpal tunnel syndrome is a sign of median nerve damage and compression is at the level of the wrist. Phalen’s test or tinnel test can be used to make the diagnosis of carpal tunnel syndrome. The nerve is compressed in the carpal tunnel and treatment can be conservative or surgical (by Incision of the flexor retinaculum) 8. Foot drop can be caused by both peroneal nerve and sciatica nerve. 9. Sciatica is a term usually used to describe the lower back pain radiating all the way down the led up to knee or below it.

ORTHOPAEDIC ANATOMY

Radial nerve
innervates All extensors of hand I.e. extension of wrist, fingers, elbows Therefore radial nerve palsy causes wrist drop Ulnar n nerve
Innervates all intrinsic hand muscles, except the LOAF which are innervates by the median nerves. Therefore ulnar n palsy if claw hand

Median nerve
LOAF L- The 2 Lateral lubricals O- Opponens pollicis A- Abductor pollicis brevis F- Flexor pollicis brevis

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1. Shoulder abduction: • Deltoid • Axillary • C5 1. Elbow flexion: • Biceps • Musculocutaneous • C5, C6 1. Elbow extension: • Triceps • Radial • C7

1. Finger Extension: • Extensor Digitorium superfacialis & profundus • Radial • C7 1. Finger flexion: • Flexer digitorium profundus & superficialis • Median & Ulnar • C8

1. Finger abduction : • First dorsal interosseous • Ulnar • T1 •

1. Thumb abductor: • Abductor Pollicis Brevis • Median • T1

1. Finger Adduction: • Second Palmar interossei • Ulnar • T1

Shoulder Muscles: •

Pulling arm backward while the hands is on waist & move elbow backwards on resistance

Rumboid muscle

•

Serratus Anterior muscles: Imagine you are pushing the a car. In this position you are using the serratus anerior muscle

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1. Supraspintus: • Suprascpular nerve. • Lifting arms sideways between 60 and 120 degrees.

1. Infraspinatus muscle: • With a flexed elbow, move the arm inwards

1. Long flexors of little and finger ring: Flexion of distal IPJ is flexor digitorum Profundus 3 & 4 DIP
Profundus PIP
Suprficialis 2. Flexor pollicis loungus: • Flexes thumb Hip flexion Hip Extension L1, L2; Iliopsoas S1; Gluteus Muscle ; Sacral plexus ; Inferior gluteal nerve Knee extension L3, L4; Femoral nerve Quadriceps muscle Dorsiflexion foot L5; Tibialis antetrior muscle ;Deep Peropneal

• • •

Knee Flexion: Hamstring muscle Sciatic nerve (foot drop) L5, S1

•

• • •

Plantar flexion of the foot: Grastrocinemeous muscle Posterior tibialis S1

Reflexes 1. Supinator
Radial nerve , C6 2. Triceps
Radial nerve, C7, Biceps – C5 Musculocutaneous nerve 3. Finger
Median, Ulnar nerves 4. Knee
Femoral, L3, L4 5. Ankle
S1, S2

DERMATOME FOR LOWER LIMB: L1
Pocket

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L2
Inner thigh L3
Knee L4
Medial malleoli L5
Lateral Dorsum of the foot S1
Sole S5
Saddle Upper limb L4 Shoulder L5 arm 6 thumb 7 Middle finger 8 Little finger

LYMPH NODES DRAINAGE

1. The cervix lymph drains into the para-aortic lymph nodes 2. Vulva lymph drains into superficial Inguinal lymph nodes ----->then into deep inguinal lymph nodes

3. Lower nodes then into deep inguinal lymph nodes

4. Body of the uterus drains into external ilia lymph nodes

5. Fundus of the uterus drains into para-aortic lymph nodes

6. Ovaries drain into para-aortic lymph nodes

7. Superior half of the rectum drains into pararectal lymph nodes --->then into inferior mesenteric lymph nodes

8. Lower half of the rectum drains into internal iliac and sacral group of LN.

9. Testes drain into paraaortic lymph nodes

10. Superficial Inguinal Lymph nodes drains fro penis, scrotum, perineum, buttock, vulva and abdominal wall below the umbilicus.

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11. Usually the superficial lymph nodes drain into then into para-aortic

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deep inguinal

then into

external iliac

and

12. Ovaries drain into para-aortic lymph nodes

13. Prostate drains into into external iliac 14. EXTERNAL ILIAC LYMPH NODES: drains from the glans of the penis, prostate, upper vagina, fundus of the bladder.

15. INTERNAL ILIAC NODES: drains from deeper perineum, urethra, buttock and back of the thigh.

16. PARAAORTIC LYMPH NODES drains from ovaries, testes and superior rectum 17. SUPERFICIAL CERVICAL LYMPH NODES: nodes: lower part of auricular and parotid region. 18. ANTERIOR CERVICAL LYMPH NODES: lower part of the larynx, thyroid gland and upper part of the trachea.

LYMPH NODES OF THE FACE SUBMENTAL LYMPH NODES: drains from the floor of the mouth, apex of the tongue and lower lip then goes to deep cervical lymph nodes..

LYMPHATIC VESSELS FO THE TONGUE -Apical of the tongue or tip =submental -Lateral margin of the tongue= submaxilary lymph nodes -basal of the tongue =superior deep cervical LN

SUBMAXILARY OR SUBMANDIBULAR LYMPH NODES= nasal cavity and gums, cheek, upper lip, lateral part of the lip, medial palpabrae commissure, lateral part of the lower lip.

SUBMENTAL LYMP NODES: lower lip and floor of the mouth and apex of the tongue.

BREAST: mainly drain into axillary lymph nodes

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TERMINOLOGIES IN EPIDEMIOLOGY 1. INCIDENCE: Is the number of new cases divided by the total population per year who are at risk of becoming a case 2. Prevalence: The proportion of people in a given population at a given point/time who had a disease

3. Mode: is the value that occurs most frequent

4. Median : is the middle value when the values are ranked. 5. Sensitivity: Is the proportion of true positives correctly identified by a test.

6. Specificity: Is the proportion of the true negatives correctly identified by the tests. Resource start date

2014-05-13 09:44

Resource end date

2024-05-13 09:44

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SAMSONPLAB ACADEMY BOW BUSINESS CENTRE BOW ROAD 153-159 E3 2SE, London EMAIL: [email protected] Tel: +447940433068

Cardiology lecture notes Chest Pain: 1.

MI (ST elevation-STEMI)

2.

Stable Angina

3.

Pneumonia

4. PE 5.

Pneumothorax

6.

Aortic dissection

7.

GERD

8.

Musculoskeletal pain

9.

Pericarditis

10.

Acute coronary syndrome

11.

Unstable Angina

Acute coronary syndrome (ACS) consists of: •

STEMI

•

NSTEMI

•

Unstable Angina

Unstable angina is angina which is occurs at rest or it has increased in frequency or duration or it is occurring with less effort than it used to happen before. It is therefore difficult to differentiate from Myocardial infarction.

NSTEMI stands for Non ST elevation myocardial infarction. This simply means that one can have myocardial infarction without ST segment elevation on an ECG i.e. normal ECG or ST depression. It is therefore difficult to differentiate from unstable angina.

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STEMI stands for ST elevation myocardial infarction. This simply means that the patient will have elevation of ST segment on an ECG. Hence before you do an ECG, this could still be difficult to differentiate from unstable angina and NSTEMI. NB: It is difficult to differentiate between unstable angina and NSTEMI using an ECG because in both cases ECG can be normal or show ST segment or T wave abnormalities may be seen, therefore you need to do cardiac enzymes to differentiate them.

The terminology Acute Coronary Syndrome (ACS) is used to describe the way these 3 conditions present. So before you can differentiate between these 3 conditions, this is the way to treat them.

TREATMENT OF ACS 1.O2 2.GTN 3.Aspirin 300mg 4. Clopidogrel 300mg 5.Morphine and Metoclopramide 6.LMWH(Enoxaparin and Dalteparin) 7.Beta-blockers – as anti angina

MYOCARDIAL INFARCTION 1. NSTEMI (NON ST ELEVATION MYOCARDIAL INFARCTION) •

Sudden onset central, crushing chest pain radiating to throat/ left arm

•

Lasting > 20 min

•

Associated with nausea & vomiting, sweating in the palms

ECG: ST depression or T wave inversion ,Troponin is raised. If no changes are seen on ECG but the cardiac enzymes are raised then it is NSTEMI We need cardiac enzymes to make the diagnosis

Symptoms I.

Central chest pain, crushing in nature, radiating to Left arm lasting greater than 20 min

II.

Complaining of nausea, vomiting, sweating

III.

Silent MI or a typical chest pain usually in diabetic patient.

IV.

May lead to LVF leading to Pul.oedema, which presents with Tachycardia, low BP and SOB.

2. STEMI ( ST ELEVATION MYOCARDIAL INFARCTION) •

Sudden onset of chest pain which is central, crushing, retrosternal

•

Radiating to left arm or neck

•

Associated with nausea, vomiting, sweating

•

ECG:

•

Cardiac enzymes are raised

•

when there is STEMI cardiac enzymes are not needed to make the diagnosis. Diagnosis is from the ECG

ST elevation or new LBBB

CLASSIFICATION OF ST ELEVATION MYOCARDIAL INFARCTION I.

ST elevation in lead II, III and AVF - indicates inferior MI

II.

ST elevation in V₁-V₂

III.

ST elevation in V₃-V₄

- indicates septal MI

IV.

ST elevation in I, aVL, V₅, V₆

- indicates ant. MI - indicates Lateral MI

Other ECG changes involve, T wave inversion & Q waves-always MI CXR may show Pulmonary Oedema in the form of bilateral fluffy opacities or it may show cardiomegaly or it may be normal

MANAGEMENT OF STEMI OR SIMPLY MYOCARDIAL INFARCTION 1. O₂

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2.

Aspirin 300 mg then 75 mg everyday

3.

Morphine iv and metoclopromide (anti sickness/ nausea)

4.

GTN sublingual

5.

Percutaneous coronary intervention ( angioplasty) or Thrombolysis if PCA is not available

When the patient Is stable 1.

Continue to give ACE- I even with normal BP

2.

Beta- BLOCKERS(anti angina)

Indication for thrombolysis 1.

Chest pain 150

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1) If signs of instability are present then give DC shock and if DC shock not helping then give IV Amiodarone. NB. DC shock is the same as electrical cardioversion. Amiodarone is used for chemical cardioversion. 2) If patient with tachycardia is stable then check if it is broad complex tachycardia (eg VT or VF) or narrow complex tachycardia. •

Narrow complex tachycardia (QRS < 0.12 secs on ECG)

•

If narrow complex tachycardia and irregular then most likely it is AF.

•

If narrow complex tachycardia and regular then it can be sinus tachycardia, Atrial flutter, WPW syndrome or atrial tachycardia. In this case perform vasovagal manoeuvre or carotid massage, if that does not help then give Adenosine.

•

If vasovagal manoeuvre/carotid massage or adenosine terminates the arrhythmia then it is AVRT (Wolf Parkinson White syndrome).

•

If vasaval manoeuvre and adenosine do not terminate the arrhythmia but just slows the rate down, then it is likely to be atrial flutter, atrial tachycardia or atrial fibrillation.

•

SVT (Supra-ventricular tachycardia) is terminology which suggests any arrhythmia arising above the ventricles.

•

It is usually difficult to differentiate between AF, Atrial flutter, Atrial tachycardia and WPW syndrome. That is why we perform vasovagal manoeuvre/carotid massage or give adenosine to slow down the heart rate so that we can read and interpret the ECG properly. If it terminates with above methods then it is WPW.

•

Broad complex tachycardia (QRS > 0.12 secs on ECG)

•

It can also be either regular or irregular.

•

If it is irregular then it is either VF (Ventricular fibrillation) or torsades de pointe. Give IV Magnesium (Mg 2+) for torsades de pointe and DC shock for VF.

•

Ventricular fibrillation usually does not present with palpitations. It presents with collapse.

•

If it is regular then it is more likely to be VT (Ventricular tachycardia). Treat patient with amiodarone unless patient is unstable in which case he needs DC shock. Initial dose for amiodarone is 300 mg.

NB: If patient with arrhythmias is unstable give DC shock no matter what type of arrhythmia it is, narrow or broad complex tachycardia.

•

If there is AVRT which involves accessory pathway E.g.

•

WPW: digoxin is CI because they block AV node not accessory pathway & make symptoms worse

Management of SVT: -most of the time they mean WPW. Valsalva manoeuvre (carotid sinus massage)

1.

No help 2)

Give adenosine 6 mg

No help 9 mg

12 mg

18 mg

NB: - 1. Or 2. Terminates AVRT (Atrial ventricular re-entrant tachycardia) and AVNRT (Atrioventricular node re-entrant tachycardia)– will bring it to normal rhythm

-Therefore if arrhythmias is controlled by 1) or 2) it means it’s WPW. 1. Or 2. will cause transient block and review whether it is AF, Atrial flutter, Atrial Tachycardia (but it will not terminate these, slow them down)

NB: - Atrial flutters medication is B- blockers i.e. metoprolol treat just like Atrial fibrillation. - Ventricular Fibrillation does not present with palpitations. It presents with collapse and is incompatible with life. - A patient with VF is usually unstable.

2. AF :

There is irregular pulse on examination

Patient experiences palpitations and this is usually a common complaint. Symptoms: SOB, chest pain, collapse, palpitations

Causes: A.

IHD (MI, Angina)

B.

Mitral valve disease esp. Mitral Stenosis

C. HTN

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D.

Heart failure

E.

Pneumonia

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F. PE G.

Atrial myxoma - tumor of heart muscle

H.

Thyrotoxicosis

I.

Alcohol

J.

Cardiomyopathy

3. Ectopic beats – usually ventricular ectopics Causes: - coffee, alcohol,smoking Management: - 1. If infrequent ectopics, manage with life style modification e.g. stop smoking,reduce caffeine,reduce alcohol. NB: Patients usually complain of missing beats or pounding in the chest

4. Atrial flutter •

Commonly secondary to valvular heart disease or IHD

•

HR 300 with 2:1 block

NB: if HR= 150 think of Atrial Flutter. NB: - VF Never presents with palpitations, it presents with collapse -Patient cannot tolerate VF -Always haemodynamically unstable -Cardioversion is the only option

5. Anxiety •

Young female

•

Palpitation, sweating, perioral paresthesia, SOB

•

CO₂ is low (PaCO₂ is decreased ) due to hyperventilation

•

PaO₂ is normal or high

6. Thyrotoxicosis/ hyperthyroidism •

Presents with AF, tachycardia, sweating, diarrhoea, palpitation

•

Wt. Loss despite good appetite, oligomenorrhoea

7. Atrial myxoma •

Benign cardiac tumour

•

May present with palpitations which resolve when sitting up but worse when lying flat

•

Weight loss, fever, may cause AF

8. Pheochromocytoma •

Catecholamine producing tumours from adrenal glands

•

Episodic (on & off) headaches, sweating, tachycardia, hypertension

•

Anxiety attacks: - tremor, palpitation

Investigations: - urinary catecholamines (which are adrenaline, Nora- adrenaline and dopamine)

Management of Brady-arrhythmias: Patients with brady-arrhythmias can also be either stable or unstable.

Signs of instability: •

Systolic BP < 90 mmHg

•

HR < 40/min

•

Heart failure

•

Reduced consciousness

•

If patient is unstable give atropine and if atropine not effective then do cardiac pacing.

•

If patient is stable then check for the risk factors of asystole (chance that heart will stop at any time) e.g. Mobitz type II block, complete heart block, recent systole or ventricular pause.

•

If any of the above risk factors present then give atropine and subsequent cardiac pacing if did not respond to atropine.

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TYPES OF ANGINA I.

Stable angina - Angina which comes with certain amount of exercise and relieved by rest. The patient can predict it. The pain usually lasts less than 20 minutes and responds to GTN.

II.

Unstable angina

III.

Decubitis angina - the patient experiences pain on lying flat

IV.

Prinzmetal/ variant angina is due to coronary artery spasm, ST elevation for a short period of time which resolves quickly. INVESTIGATION OF STABLE ANGINA

•

Resting ECG

•

If resting ECG is normal then observe, If abnormal or shows blockage then do angiography

MANAGEMENT1. Aspirin-LOWER DOSE 2. Beta- blockers e.g- atenolol 3. GTN sub lingual (Nitroglycerine) 4. Calcium channel blockers (amlodipine or diltaizem) 5. Statin if cholesterol> 4 mmol/ L 6. If symptoms not controlled then add

Nicorandil

(k⁺ channel activator)

7. Life style modification-stop smoking, reduce alcohol intake, wt.loss. 8. Prinzmetal Angina: Treat with Calcium channel blocker (1st choice) i.e. amlodipine or diltiazem

Heart Failure: Types: 1. Left ventricular failure (LVF) 2. Right ventricular failure (RVF) 3. Congestive heart failure (CHF) - a combination of both left and right ventricular failure

Left ventricular failure (LVF) •

Dyspnoea

•

Orthopneoea

-

PND (paroxysmal nocturnal dyspnea)

-

Pinky frothy sputum

-

(Pulmonary Oedema)

-

Cardiac wheeze

Right Ventricular Failure R(VF) •

Peripheral oedema

•

JVP/ engorged neck veins

•

Ascites

•

Peripheral edema

•

hepatomegaly

LVF+ RVF = CCF (congestive cardiac failure)

Investigation:echocardiogram - to see LV function Chest X-Ray
cardiomegaly, bilateral fluffy opacities on the chest x-ray studies indicates pulmonary oedema

Heart failure can also be classified into Acute and Chronic Heart Failure

1. Acute HF 1. Commonly due to Left ventricular failure leading to pulmonary oedema

Treatment of Pulmonary Oedema 1. Sit patient up in bed 2. O₂ 3. IV Diamorphine+ metaclopromide

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4. IV Furosemide (main Rx) 5. GTN if BP greater than 100

2. Chronic HF

Treatment of chronic HF 1.

diuretics
Give loop diuretics e.g.
furosemide

-If not helping add thiazide diuretic ( e.g bendroflumethiazide) NB: spironolactone if k⁺ < 3.2mmol k 1.

ACE- I eg lisinopril,enalapril esp if there is LV dysfunction

Side Effect: Dry cough If cough problematic then consider ARBs (Angiotension receptor blocker) e.g.
condesatan or losartan 1.

Beta- blockers
e.g carvedilol

2.

Spironolactone
if still symptomatic despite all the above Rx.

3.

Digoxin
if AF with HF then add digoxin

4.

Isosorbide mononitrate to reduce the preload of the heart (vasodilation)

HYPERTENSION CAUSES:

1. Essential hypertension-common in 95%, usually elderly patients 2. Coarctation of Aorta - Hypertension, young patient, chronic headache, radiofemoral delay 3. Polycystic kidney disease-bilateral loin pains, haematuria, hypertension, renal failure, family history. 4. Renal artery stenosis- Hypertension, abdominal bruit. ACE-I contraindicated. 5. Pheochromocytoma- episodic headaches, episodic hypertension, flushing palpitations all intermittent 6.Conns Syndrome- Hypertension, low potassium, due to over production of aldosterone, high sodium 7.Cushing Syndrome - Typical features are an obese patient usually central obesity, hypertension, excessive facial hair, abdominal striae

Essential Hypertension •

95% of all cases of hypertension

•

Usually asymptomatic until end organ damage eg hypertensive retinopathy, nephropathy

•

When to treat? Only when BP is greater than 160/100 mmHg

Classification of Essential HTN Systolic Normal

Diastolic

200ms = 1st Heart Block

• If certain QRS complex missing then 2nd Heart Block

if Heart Rate 3 small boxes

• If QRS i. Positive = RBBB

ii. Negative = LBBB

• RBBB + LAD + first degree heart block = Trifas Trifasc ifascicular block

• RBBB + LAD LAD = Bifasc Bifascicular (i.e. R + posterior branch affected) affected)

• New LBBB plus chest pain= pain= MI

• If LBBB = No further interpretation of an ECG

9. ISCHAEMIA • Q Wave = Old /E /Evolving MI • Elevated ST = acute MI or Pericarditis(wide spread ST elevation)

• ST depression i. Digoxin toxicity ii. Ischaemia

• T-wave inversion i. Acute ischaemia

ii. Old infarct (only if exists with QQ-

wave)

• Tall TT-wave = HYPERKALAEMIA

10.

Walls:

aVF, II and III =inferior MI, MI, I, AVL, AVL, V5, V6=lateral MI V1V1-V6, aVL, aVL, I= anterior anterior lateral MI V1V1-V4 =Anterior MI V1V1-V2=septal V2=septal MI

11.

HYPER YPERTROPHY (USE CHEST LEADS) 2. R + S ≥ 35mm 35mm = Left Left Ventricular Hypertrophy (LVH) 3. Tallest R in (V4 or V5) V5) plus deepest S (V1 or V2)

4. Peaked PP-wave = P. Pulmonale = ↑ Right atria (R atrial strain)

5. Toothed (biphasic) PP-wave = P Mitrale Mitrale = ↑ Left atria (Left atrial strain)

6. Dizziness, syncope, fainting on exercise = aortic stenosis

7. New LBBB plus chest pain= pain= acute MI until proven otherwise (check previous

ECG & compare the two)

8. If murmur or new AF = ECHO 9. If dizziness on exercise = ECHO 10. LAD is associated with LBBB & LVH

11. Common cause of P Mitrale = Mitral Stenosis 12. If LAD & No LVH or LBBB or RBBB
think of L anterior hemiblock

13.

WPW 1. if wide QRS is in V1
then the

accessory pathway is on the left left side)

2. if wide wide QRS in V6
then the

accessory pathway is on the Right

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Endocrinology PLAB 1 Notes

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Endocrinology

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ENDOCRINOLOGY SAMSONPLAB ACADEMY Bow Business Centre Bow Road 153-159 E3 2SE, London Telephone: +44(0)2089800039 Mobile: +447940433068 Email: [email protected] Contents: 1. Diabetes Mellitus Acute Complications a. Hypoglycaemia b. Diabetic Ketoacidosis c. Hyperglycaemic hyper-osmolar non ketotic coma Chronic Complications a. Microvascular b. Macrovascular 2.Hyperthyroidism a. Subclinical Hyperthyroidism 3. Hypothyroidism a. Secondary Hypothyroidism b. Tertiary Hypothyroidism c. Sub Clinical Hypothyroidism 4. Parathyroidism a. Hyperparathyroidism b. Hypoparathyroidism 5.Adrenal Glands a. Cushing Syndrome b. Addison’s Disease

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c. Conn’s Disease d. Pheochromocytoma 6. Acromegaly 7. Syndrome of In Appropriate Anti Diuretic Hormone 8. Hyperprolactinemia 9. Diabetes Insipidus 1. DIABETES MELLITUS – This is high serum blood glucose

DM results from lack or reduced effectiveness of endogenous insulin. It is imperative that a diabetic person having hypertension should have it well controlled. TYPE 1 DIABETES

• • • • • • •

Usually juvenile onset Common in young patients It is due to absolute deficiency of insulin An autoimmune condition in which there is destruction of the B cells of the pancreas Symptoms: Polyuria, Polydypsia, Weight loss, Diabetic Ketoacidosis First presentation can be Diabetic Ketoacidosis There could be history of other autoimmune conditions like Addison’s disease, Thyroid disease and Pernicious Anaemia • Antibodies e.g. anti-glutamic acid decarboxylase (GAD) antibodies and islet cell antibodies

TYPE 2 DIABETES

• Usually occurs in the adults mostly in Asian men and above the age of 40 years, most are obese • Is due to insulin resistance and relative insulin deficiency • Often it is asymptomatic and may first present with complications like diabetic retinopathy, nephropathy and neuropathy

• RISK FACTORS: Pregnancy, obesity, polycystic ovarian syndrome (PCOS), renal failure, lack of exercise DIAGNOSIS: To make the diagnosis of diabetes, you need to consider the following: 1. If the patient is asymptomatic do the blood tests twice, either:

• Fasting glucose >7.0 OR • Random blood glucose> 11.0 confirms the diagnosis Fasting glucose 35 mmol/l 3. Plasma osmolarity >350 mosm/kg 4. Ph is normal 5. No ketones in the urine Symptoms:

1. Dehydration 2. Lethargy, weakness, polyuria, polydipsia, progressive loss of consciousness over days Treatment: IV fluids (normal saline) an Insulin

CHRONIC COMPLICATIONS OF DIABETES

1. MACROVASCULAR COMPLICATIONS a. Heart - Myocardial Infarction: Usually patient has silent Myocardial Infarction (MI) or atypical chest pain due to neuropathy. b. Brain - TIA/Stroke due to atherosclerosis. c. Peripheral vascular disease - atherosclerosis leads to intermittent claudication. Pain comes on walking and after a short rest it goes away.

2. MICROVASCULAR COMPLICATIONS Diabetic retinopathy

A. Background - Micro-aneurysms, dot and blot haemorrhages and hard exudates B. Pre-Proliferative - Micro-aneurysms, dot and blot haemorrhages, hard exudates and soft exudates (cotton wool spots)

C. Proliferative - Micro-aneurysms, dot and blot haemorrhages, soft and hard exudates, new vessel formation (neovascularization)

• New vessel formation leads to bleeding which may cause retinal detachment which comes as a sudden loss of vision and the patient complains as a curtain coming down. Cataract formation is earlier. Diabetic Maculopathy - This is when changes develop in the macula Vitreous haemorrhage - This is when there is bleeding in the vitreous. The patient usually complains of floaters.

Diabetic Nephropathy

• Micro-albuminuria- loss of >300mg/day of protein. • It is a big risk factor of IHD and stroke therefore it needs treatment. • In people who are diabetic, the target BP is ≤ 130/80 and if there is micro-albuminuria then target BP ≤125/75. Micro-albuminuria leads to diabetic nephropathy and eventually renal failure if not treated. In renal failure insulin sensitivity increases and insulin metabolism decreases therefore insulin needs to be reduced to avoid hypoglycaemic attacks. Diabetic Neuropathy

1. 2. 3. 4.

Peripheral neuropathy (somatic neuropathy) is usually symmetrical in a form of gloves and socks. rd

th

th

Mono neuropathy e.g. 3 , 4 and 6 nerve palsy. Autonomic neuropathy will cause vasovagal syncope, diarrhoea, postural hypotension or urinary retention. Amyotrophy – progressive wasting and weakness of muscles especially the quadriceps muscles.

2. PITUITARY GLAND

Anterior Pituitary produces Growth hormone (GH), Gonadotropins: Follicle stimulation hormone (FSH) & Leutenizing hormone (LH), Prolactin (PRL), Thyroid stimulating hormone (TSH), Adrenocorticotrophic hormone (ACTH) Posterior Pituitary stores Oxytocin and ADH (Anti-diuretic hormone) • Oxytocin acts on the uterus and causes contraction. • ADH acts on the kidneys and cause urine retention. NB: The ANTERIOR PITUITARY PRODUCES hormones and the POSTERIOR PITUITARY STORES hormones. Hypopituitarism

Hormones are affected in this order: GH, FSH & LH, PRL, TSH, ACTH Causes are at 3 levels:

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1. Hypothalamus: Kallman’s syndrome (isolated FSH LH deficiency with anosmia and colour blindness), tumour, inflammation, infection

1. Pituitary stalk: Trauma, surgery, compression by a mass lesion (eg. due to a craniopharyngioma), carotid artery aneurysm

1. Pituitary: Tumour, irradiation, inflammation, autoimmunity, ischaemia (eg. Sheehan’s syndrome due to post partum haemorrhage) Clinical features: depends on the hormone that is deficient and the underlying cause. Investigations: Check for the specific hormones and look for the underlying cause eg. MRI for pituitary tumour Treatment: Hormone replacement and treatment of the underlying cause.

3. HYPERTHYROIDISM

Hypothalamus ↓ Thyroid Releasing Hormone (TRH) ↓ Pituitary ↓ Thyroid Stimulating Hormone (TSH) ↓ Thyroid gland releases: T3 and T4

SYMPTOMS OF HYPERTHYROIDISM

1. Weight loss, tachycardia, diarrhoea, oligomenorrhoea, irritability, heat intolerance, tremors, sweating and weight loss despite increased appetite, atrial fibrillation/sinus tachycardia

2. Typical signs of Graves disease are exophthalmus, ptosis, diplopia, lid retraction, lid lag CAUSES:

1. GRAVES DISEASE It is an autoimmune disease. Antibodies resembling TSH are formed and act on the thyroid and stimulate production of T3 & T4. It is associated with other autoimmune disease like type 1 diabetes, Addison’s disease, Vitiligo. There is diffuse enlargement of the thyroid gland. There is bruit and eye signs e.g. diplopia, exophthalmus. Treatment: Carbimazole. In pregnancy use propylthiouracil. Give beta blockers if no contraindications like asthma.

1. TOXIC ADENOMA It is a benign tumour of the thyroid gland and it produces thyroxine. It is a solitary adenoma, which means there will be a lump in the thyroid which moves on swallowing. Treatment is radio-iodine.

3. TOXIC MULTINODULAR GOITER There are multiple nodules. Treatment is Carbimazole and radiotherapy

1. SUBACUTE THYROIDITIS - This is also known as De-quervain’s thyroiditis The cause is viral infection ie. Upper Respiratory Tract Infection. The thyroid is usually painful and enlarged. Treatment is analgesia or observation

1. MEDICATIONS: Amiodarone, thyroxine & lithium • For amiodarone, the patient will be on treatment for arrhythmia (SVT and VT) • For thyroxine, it is usually patients with hypothyroidism and on replacement therapy with levothyroxine • For Lithium these are usually patients being treated for bipolar mood disorder

1. ECTOPIC TISSUE- this is thyroxine produced by anywhere else other than the thyroid gland. INVESTIGATIONS:

1. T3, T4, TSH 2. TSH Receptor antibodies

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3. If there is a mass in the neck then USS: if the mass is solid then do FNAC and if the mass is cyst then do surgical removal.

4. Isotope scan=to decide if it is a hot nodule or cold nodule. Hot nodule - usually indicates a benign adenoma. It accumulates iodine as it manufactures thyroxine. Cold nodule is usually cancer. It does not take up the contrast.

SUBCLINICAL HYPERTHYROIDISM This hyperparathyroidism with low TSH or symptoms but normal T3 & T4. Treatment is observation Medical treatment is needed only if TSH 0.1 or symptoms of AF, weight loss Treat with carbimazole if treatment required 4. HYPOTHYROIDISM

CAUSES:

1. Hashimoto’s Disease (Thyroid is diffusely enlarged) It’s an autoimmune disease and is associated with pernicious anaemia, Diabetes mellitus type 1, Addison disease. Antibodies: anti-peroxidase, Anti-thyroglobulin, anti-microsomal antibodies (thyroid gland is small)

1. Primary Atrophic Hypothyroidism Diffuse infiltrate, which leads to atrophy of the thyroid. It is an autoimmune disease. There is no goitre.

1. Iodine Deficiency Common in Africa where water is not iodized.

1. Thyroidectomy 1. Radio-iodine Therapy 1. Medications Carbimazole, Lithium (do TFTs and U& E), Amiodarone SYMPTOMS OF CLINICAL HYPOTHYROIDISM

1. 2. 3. 4. 5.

Weight gain, bradycardia, constipation Cold intolerance, Menorrhagia, tiredness, hoarseness, dementia Toad like face, dry skin Goitre Cholesterol raised.

SECONDARY HYPOTHYROIDISM The cause is low TSH due to problems in the pituitary. TERTIARY HYPOTHYROIDISM This is due to low TRH in the hypothalamus. Treatment: Levothyroxine SUBCLINICAL HYPOTHYROIDISM High TSH, normal T3 & T4. Treatment is observation, only treat if TSH > 10 or previous disease or other associations like vitiligo, DM type 1, pernicious anaemia or if there are positive antibodies. Use thyroxine if treatment is required. SUBCLINICAL THYROID DISEASE TSH High

T3 and T4 Normal

S u b c l i n i c a l Hypothyroidism

TSH Low

T3 and T4 Normal

S u b c l i n i c a l Hyperthyroidism

TSH High

T3 and T4 Low

C l i n i c a l Hypothyroidism

TSH Low

T3 and T4 High

C l i n i c a l Hyperthyroidism

5. PARATHYROID GLAND

1. 2. • • •

Produces Parathormone, the main function of which is to increase calcium in the blood. Parathormone increases the production of active vitamin D and in turn vitamin D does the following actions. Increases reabsorption of calcium from the kidney Increases absorption of calcium from the gut Increases release of calcium in from the bones.

THE OVERAL EFFECT OF PARATHORMONE IS TO INCREASE CALCIUM IN THE BLOOD.

HYPERPARATHYROIDISM 1. PRIMARY HYPERPARATHYROIDISM

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• The commonest cause of hyperparathyroidism is the adenoma of the parathyroid, usually solitary adenoma. • The second cause is hyperplasia of the parathyroid. SYMPTOMS OF HYPERPARATHYROIDISM are mainly due to hypercalcaemia. These are weakness, tiredness, depression, polyuria, polydipsia, confusion, thirst and abdominal pain and constipation. Parathyroid adenoma is usually associated with MEN1 (Multiple Endocrine Neoplasia). MEN syndrome consists of MEN 1 Pancreas tumour =gastrinoma Parathyroid adenoma Pituitary adenoma MEN 2a Thyroid tumour Adrenal adenoma Parathyroid adenoma MEN 2b Thyroid Adrenal Parathyroid Mucosal neuromas Zollinger-Ellison disease is multiple ulcers in the stomach, duodenum and small intestine, which are poorly responsive to PPI and caused by Gastrinomas occurring as MEN 1. INVESTIGATIONS FOR HYPERPARATHYROIDISM

1. 2. 3. 4.

Serum Calcium Parathyroid level Bone scan for osteoporosis USS of the parathyroid and thyroid

Treatment: SURGERY

2. SECONDARY HYPERPARATHYROIDISM Causes:

1. Deficiency of vitamin D 2. Chronic renal failure→ Active vitamin D is formed in the kidney. 3. Malabsorption Treatment: Active vitamin D and calcium.

HYPOPARATHYROIDISM CAUSES:

1. Thyroidectomy: Usually during thyroidectomy the parathyroid glands are removed as well. 2. Symptoms are those of hypocalcaemia ie. tetany and peri-oral parasthesia Chovestek sign- when tapping on the angle of the jaw there is twitching of the muscles of the face. Trousseau’s sign- when you tie the BP cuff on the arm there is flexion of the forearm and fingers. This sign is also called carpal pedal sign. Treatment:

1. Calcium Gluconate intravenously if severe 2. Calcium supplements if mild (Oral Ca tablets)

1. ADRENAL GLANDS HYPOTHALAMUS ↓ Corticotropin Releasing Hormone (CRH) ↓ PITUITARY ↓ ACTH ↓ ADRNAL GLAND {Glucocorticoid (CORTISOL) Mineralocorticoid (ALDOSTERONE) Androgens} Catecholamine’s (adrenaline, noradrenaline) DYSFUNCTION OF ADRENAL GLANDS

A. HYPO FUNCTION OF THE ADRENAL GLANDS

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Addison’s Disease - low production of cortisol mainly due to autoimmune disease and infection e.g. tuberculosis

A. HYPER FUNCTION OF THE ADRENAL GLANDS 1. 2. 3. 4.

Pheochromocytoma- tumour of the adrenal glands from the medulla. Conn’s disease- adenoma of the adrenal cortex producing aldosterone Cushing’s syndrome- see below Virilization- increased production of the androgens

CUSHING’S SYNDROME This is excess of cortisol from any cause

CAUSES:

1. Cushing disease This is high cortisol due to pituitary adenoma This is the commonest cause Cushing disease is when the tumor is located in the pituitary and produces high ACTH which stimulates the adrenal gland to produce high cortisol

1. Adenoma of the hypothalamus This leads to high production of corticotrophin releasing hormone- high production of ACTH leads to high production of cortisol in the adrenal glands.

1. ACTH produced by lung cancer usually caused by small cell lung cancer 1. Iatrogenic i.e. patient on treatment for Addison’s disease or asthma or COPD. 1. Adrenal adenoma - this tumour of the adrenal glands. Symptoms of Cushing Syndrome:

1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12.

Weight gain Mood changes Central obesity Acne Amenorrhea or irregular menstrual Hirsutism Moon face Buffalo hump Impaired glucose tolerance test Hypertension Abdominal striae Acanthosis Nigricans

DIAGNOSIS

• 1st LINE INVESTIGATIONS (SCREENING TEST) Overnight Dexamethasone suppression test or 24 hour urinary free cortisol.

• 2nd LINE INVESTIGATION (CONFIRMATION TEST) st

nd

If any of 1 line test is positive go for 2 line. Which are 48hr Dexamethasone suppression test OR Midnight cortisol/diurnal cortisol

• 3rd LINE INVESTIGATION (LOCALIZATION TEST): To find where is the lesion. Plasma ACTH: It is usually not detectable in blood.

A. If it is increased or detectable- (May be Ectopic or may be Pituitary cause). Perform high dose Dexamethasone suppression test.

1. If cortisol is suppressed, the diagnosis is Cushing disease. Do MRI of the pituitary because the most likely locations the pituitary gland.

2. If cortisol is not suppressed, the diagnosis is likely to be due to an ectopic tumour. Do CT scan to locate the carcinoid tumour. B. Decreased or undetectable - do CT Scan of adrenal glands. If no mass is visible on the CT scan then perform Adrenal Vein Sampling. TREATMENT - Surgery - If iatrogenic - Remove the cause.

ADDISON’S DISEASE- Low Cortisol Causes

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1. 2. 3. 4. 5. 6.

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TB (Most common in developing world) Autoimmune (Commonest Cause) Metastasis Steroid HIV Waterhouse Friderichsen Syndrome (Haemorrhage in the adrenal gland if patient has meningococcemia)

Symptoms

1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11.

Fatigue Abdominal Pain Nausea Vomiting Hypotension (hyperkalemic hypotension) Weight loss Anorexia Diarrhoea Constipation Hyperpigmentation Vitiligo

INVESTIGATIONS Short ACTH Stimulation test (Synacthen test) - Definitive Investigation. Other investigations: U&E = K+ increased, Na+ decreased, Glucose decreased. RISK FACTORS

1. 2. 3. 4.

Surgery Infection Sepsis Trauma

TREATMENT

• Replace steroids • Hydrocortisone • If Postural Hypotension- Fludrocortisone

CONGENITAL ADRENAL HYPERPLASIA

Congenital autosomal recessive disease characterised by cortisol deficiency, with or without aldosterone deficiency and androgen excess. It has 2 types: classic and non-classic. CLASSIC: severe form. It’s either salt losing or non-salt losing Symptoms: FEMALES: Classically presents with ambiguous genitalia with enlarged clitoris and one combined sinus instead of a separate urethra and vagina. May experience salt-losing adrenal crisis. MALES: classically present with no signs at birth.

• Those with salt-losing form typically present at 7-14 days with vomiting, weight loss, lethargy, dehydration, hyponatraemia and hyperkalaemia.

• Those with non-salt-losing form present with virilisation at age 2-3 NON-CLASSIC: mild or late-onset form, they present with hyperandrogenism in later childhood and early pubarche, infertility, hirsutism, amenorrhoea, polycystic ovaries. Investigations: Renal function, electrolytes, blood glucose, serum 17-hydroxyprogesterone, corticotropin stimulation test, pelvic ultrasound, bone age

Treatment: Classic: Standard hormone replacement, these include glucocorticoids, mineralocorticoids Non-classic: Treatment only symptomatic.

CONN’S DISEASE This is excess aldosterone, which causes Na+ retention CAUSES:

1. Adrenal adenoma 2. Bilateral hyperplasia SYMPTOMS:

1. K+ decreased

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2. 3. 4. 5. 6. 7. 8.

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Na+ Increased or normal Weakness Cramps Polyuria Polydipsia Parasthesias HTN

INVESTIGATIONS

1. Aldosterone/ Renin ratio altered or altered Serum Aldosterone 2. CT adrenal TREATMENT

1. Hyperplasia- Medicine (Spironolactone/Amiloride) 2. Adenoma- Surgery (Spironolactone given 4wks pre-op PHEOCHROMOCYTOMA This is due to increased effect of catecholamines, usually due to adrenal tumour. Rule of 10 10% Malignant 10% Bilateral 10% Extra-adrenal 10% Children 10% Familial Increased Catecholamines, associated with MEN-2. SYMPTOMS:

1. 2. 3. 4. 5. 6. 7. 8.

Episodic Hypertension and headaches Anxiety Sweating Palpitation Flushing Nausea Vomiting Abdominal pain Episodes or intermittent symptoms INVESTIGATIONS:

• 24 hours urinary collection for Catecholamines/Metanephrines TREATMENT:

A. CRISIS: i. Phentolamine ii. Labetalol A. STABLE PATIENT: i. Alpha- blocker (Phenoxybenzamine) followed by ii. Beta- blocker (Propranolol) Surgery is done after 2 weeks of BP control. Treatment. Surgical removal of adenoma

7. ACROMEGALY

1. Increased growth hormone (GH) 2. Pituitary tumour (tumour compressing on the optic chiasma) Hypothalamus ↓ Growth Hormone Releasing Hormone (GHRH) ↓ Pituitary ↓ Growth Hormone ↓ Promotes muscle and bone growth SYMPTOMS

1. 2. 3. 4. 5. 6. 7.

Increase in ring & shoes size Spade like hands Widespread teeth Hoarse voice Carpel tunnel syndrome Excessive sweating Visual field defect→Bi-temporal Hemianopia

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8. Coarsening of facies 9. Prognathism 10. Macroglossia COMPLICATIONS

1. 2. 3. 4.

Impaired Glucose Tolerance Test Increase BP Cardiomegaly, Hypertrophy Increase IHD

INVESTIGATIONS:

1. Definitive- OGTT (Oral glucose tolerance test) 2. MRI of the pituitary gland 3. Serum insulin like growth hormone TREATMENT: Surgery.

8. SIADH -Syndrome of Inappropriate Anti Diuretic Hormone

This is due to overproduction of ADH which leads to reduced production of urine. Symptoms:

• Water Retention leading to hyponatraemia and hypertension • Confusion, nausea, and seizure. CAUSES:

1. 2. 3. 4.

Lung cancer- Small cell lung cancer Pancreas Cancer Prostate Cancer As a complication of Meningitis and Head Injury

DIAGNOSIS: Urine Osmolarity over than 500 mosmol/kg Plasma Na+< 125 mmol/kg, plasma osmolality BC= positive test = means normal or sensory neural deafness - BC>AC= negative test
conductive deafness - Rinne positive on both sides and weber equal on both sides mean normal. - Rinne positive on both sides but weber laterizes to the other side mean sensory neural deafness on the opposite sides. -

Rinne negative on one side and weber laterizes to the same side means conductive deafness on that side.

2. Weber test - In the middle
normal (or equal on both sides) - Localizes to affected ear => conductive deafness on that side - Lateralizes to one side means sensory neural deafness on the opposite side. NB: Rinne's test suggets and weber's test confirms. Neaonatal hearing screening test: 2 tests are used n the UK to screen all the neonates. 1) Automated oto-acustic emissions (AOAE) and 2) Automated auditory brainstem response (AABR). These test are done between day 10 and 14. For babies who did not require special care usually uses Automated oto-acustic emissions. Babies not passing this test are given the

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AABR. And if the test is not passed the n the baby is referred for audiological assessment. Pneumonic: CSSO: Conductive deafness same side, Sensory neural Opposite side. (Which means for conductive deafness Weber’s goes on the same side and for sensory neural Weber’s goes on the opposite. 3. Infection of the Pinna Localised infection of the pinna treat with antibiotics such as co-amoxiclav but if there is cellulitis treat with cefuroxime and metronidazole 4. Otitis Externa This is a common infection in ENT. There is discharge, redness and swelling of the ear but the tympanic membrane is normal. Risk factors: Swimming, Diabetics and Psoriasis). History of travel abroad for a holiday where possibly patient was swimming. If there is history of travel for a holiday it means there is chance that he could have been swimming in the rivers Investigation: swab of discharge Treatment: Gentamicin eardrops and hydrocortisone drops. If you have an option with only Gentamicin drops you an also choose it. 5. Acute Otitis media This is a very common condition. Almost everyone will suffer with acute otitis media during their lifetime. Signs and symptoms may include a preceding URTI, severe and progressive otalgia, or a discharge this is usually associated with a resolution of the otalgia. A diagnosis is made by taking a history, examining the tympanic membrane (which is red), and taking the patient’s temperature. In viral acute otitis media the tympanic membrane is pink. In this case antibiotics are not needed just give analgesia. Treatment for acute otitis media is controversial. Systematic review suggests treatment with analgesia only. However, these reviews may have included a high proportion of viral ear infections where antibiotics would not be expected to be useful. Management 1) Give analgesia in all cases. 2) Give oral antibiotics for one week such as co-amoxiclav PO or simply amoxicillin. 3) Warn the patient that the discharge may continue for 1 week 4) When the infection has resolved always check that the tympanic membrane has returned to normal. 5) If viral give analgesia. Recurrent infections of the middle ear These must be differentiated from one persisting infection. Treat any acute infections actively as above. If the patient has more than 5 infections in 6 months, then consider alternative treatment such as grommet insertion or a prolonged course of antibiotics. Treatment Medical – consider prophylaxis with Trimethoprim (TMP) / Sulfamethoxazole (SMX) syrup – 2mg/kg TMP and 10mg/kg SMX as a single nightly dose PO for 3 months. Surgical – if there is an effusion or glue ear has been present for longer than 3 months consider grommet insertion especially if there is effusion. AOM + Effusion = Glue Ears and the treatment is grommet. All treatment needs monitoring – use an infection diary to record episodes of infection pre- and post-treatment.

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Caution Acute otitis media is often misdiagnosed. Children with nocturnal earache often have glue ear/ Eustachian tube dysfunction. The tympanic membrane may be red or infected but there is no discharge and the pain resolves very quickly upon walking. Complications of Acute Otitis Media 1. Chronic infection An infection may persist and become chronic. This may be due to resistant bacteria. Use a broad-spectrum antibiotic such as ciprofloxacin. Consider myringotomy (making small hole in the TM) for the relief of symptoms or to obtain microbiological information. 2. Facial nerve palsy (7th Nerve palsy) 10% of people have a dehiscent facial nerve. This may result in a facial nerve Palsy when the bone covering is absent over the nerve. This may result in a facial nerve irritation and palsy secondary to the middle ear inflammation. The patient must be admitted to hospital and given IV antibiotics, e.g. Cefuroxime. Also consider steroid therapy, Prednisolone 1mg/kg per day, if there is total facial paralysis, to be continued for a week. Consider Myringotomy and grommet insertion if the condition fails in 24 hours. 3. Acute Mastoiditis This is an infection of the mastoid air cells, which will lead to a severe earache with tenderness, swelling and redness behind the pinna. The pinna also be pushed forwards (displaced) making it look more prominent. Investigation: CT scan Treatment: Admit and Intravenous antibiotics (Co- amoxiclav)

4. Chronic perforation of the tympanic membrane Repeated infections, which perforate the tympanic membrane, can lead to chronic perforation. Usually there is ear, which is followed by purulent discharge, and then the pain disappears. Discharge = Resolving Earache 5. Sensorineural hearing loss (SNHL) Rarely, toxins can spread to the inner ear (vestibulocochlear nerve) to produce a sensorineural hearing loss (vestibulocochlear nerve) 6. Vertigo Infection near the lateral semicircular canal can produce a para –labyrinthitis. This can cause a spectrum of vestibular disturbance ranging from mild unsteadiness to disabling vertigo. 7. Glue ear/otitis media with effusion-this is common in children. Glue ear is caused by a combination of exposure to infection and a non-functioning Eustachian tube. Almost 8 out of 10 children will have glue ear at some time during childhood. The incidence of glue ear decreases with age as the immune system develops and the Eustachian tube function improves. The signs and symptoms of glue ear can include: decreased hearing, recurrent ear infection, poor speech development, failing performance at school and sometimes, antisocial behaviour. It causes conductive hearing loss. Risk factors 1) Smoking parents 2) Bottle feeding

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3) Day-care nursery 4) Cleft palate 5) Atopy (eczema, asthma, hay fever) 6) Down syndrome

Investigations 1) Full history and examination (including the palate) 2) Age appropriate audiometry (conductive hearing loss) and tympanometry (to check pressure). Management 1) Hearing disability – how the child is coping with their hearing problem socially and at school is more important than the actual level of hearing loss. 2) Appearance of tympanic membranes – if there is gross retraction, intervention may be needed to avoid retraction pocket formation. 3) Grommet (tympano Tube) Treatment There are three options: 1) Watchful waiting- this should apply to all patients for 3 months as glue ear will resolve in 50 % of cases. 2) Hearing aid – there is a window of opportunity at 4-8 years of age. It is noninvasive, but may lead to teasing at school 3) Insertion of grommets 8. Chronic suppurative otitis media without cholesteatoma This common condition is associated with Eustachian tube dysfunction with or without an infection in the mastoid. As with other ear disease, its prevalence continues despite antibiotics. The sighs and symptoms of chronic suppurative otitis media may include persistent recurrent otorrhoea, perforation in the tympanic membrane (usually central), and no cholestetoma present. Risk factors 1) Smoking patient 2) Smoking parents 3) Acute otitis media 4) Decreased immunity Investigation 1) Full history and ENT examination 2) Microscopy of the eardrum with aural toile (washing) 3) Swab for microbiology Management 1) Give appropriate topical and system antibiotics based on the swab result. The condition may settle with antibiotics and water precautions. 2) Perform regular cleaning of the ear using microsuction –aural toilet. 3) Persistent infections may need surgery

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4) Myringoplasty-repair of the perforated tympanic membrane. 5) Cortical mastoidectomy (debridement) 9. Chronic suppurative otitis media with cholesteatoma This is often divided into congenital and acquired forms of the condition: Congenital cholesteatoma results from an abnormal focus of squamous epithelium in the middle ear space, i.e. a dermoid. Acquired cholesteatoma most often results from chronic Eustachian tube dysfunction. It was hoped that the incidence of this condition would have changed with the advent of antibiotics. Unfortunately, the disease continues and can present at any age. Signs and symptoms may include recurrent otitis media with a mucopurulent discharge, hearing loss, facial nerve palsy, and vertigo. Development of a cholesteatoma Initially squamous epithelium migrates out of the sac with ease, but as it enlarges the squamous epithelium builds up and can no longer escape. If infection supervenes on the impacted squamous epithelium/keratin, then lytic enzymes are released causing destruction of local structures. It is normally in the attic of the ear. Investigation: CT scan of the temporal bone to look for pneumatisation of mastoid or erosion of scutum. Management: usually surgical treatment 6. HEARING LOSS=DEAFNESS The aetiology of hearing loss can be determined by careful consideration of the patient‘s history, a clinical examination, and the findings of special investigations. The age of onset of the patient’s hearing loss is important, as is any family history of hearing loss. Classification of patients presenting with hearing loss Acquired Congenital 1. Prebyacusis Syndromic 2. Noise-included hearing loss Non-syndromic 3. Idiopathic sudden hearing loss 4. Autoimmune hearing loss 5. Vascular causes 6. Ototoxity 7. Non-organic hearing loss 8. Otosclerosis

1. Otosclerosis

Here new bone is

formed around the stapes footplates,

which leads to its fixation and consequent

conductive hearing loss.

This condition is usually common in pregnancy. It manifests as slowly progressive hearing loss, usually beginning in the patient’s twenties. There is usually a family history of the condition. It is bilateral, common in pregnancy The patient may have difficulty hearing when chewing and may have problems with quiet conversation. Some 69-80% of patients have tinnitus. Accelerated progression is often seen during pregnancy. Bilateral conductive hearing loss. It usually begins in the twenties. Incidence

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• The female to male ratio is 2:1 • Temporal bones have evidence of otosclerosis. • The population have a clinical manifestation of the disease. • The condition is bilateral in 70% of patients. • 50% of patients with otosclerosis have a family history. Investigations • Check for a normal mobile intact tympanic membrane. • Consider a CT scans – this may help to exclude other bony abnormalities of the middle ear causing ossicular fixation. Differential diagnosis Paget’s disease - this is the only other bony lesion which involves the middle ear. Here there is increased alkaline phosphatase and a mixed hearing loss (conductive or sensory neural sensory loss) Osteogenesis imperfecta – (also known as Van der Hoeve syndrome) leads to mixed hearing loss with blue sclera. There is frequently a history of multiple bony fractures with no history of trauma. Treatment The options are: • No treatment • Hearing aid as an initial treatment. • Surgery- stapedectomy after a 3–month trial of hearing aid

2. Presbyacusis This term describes a decreased peripheral auditory sensitivity. It is usually age-related, and affects men more than women. Usually starts at the age of 40. Signs and symptoms This condition shows itself as bilateral, progressive, symmetrical sensorineural hearing loss, with no history of noise exposure. Decreasing central auditory discrimination leads to phonemic regression. Investigations 1) Otoscopy 2) Pure tone audiogram Management The patient may be given counselling and advice about hearing loss, and given a hearing aid where the symptoms are troublesome

3. Noise-induced hearing loss This is defined as damage to the inner ear caused by exposure to loud noise. There is a relationship between the volume of sound and its duration, which causes damage. Signs and symptoms The patient will usually present with bilateral and symmetrical hearing loss. There may be a noise-induced temporary threshold shift (TTS) – for example. Hearing may improve over the weekend if the problem is noise at work.

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The patient may have difficulty hearing in background noise or they may have tinnitus. Bilateral sensory hearing loss (SNHL) Investigation • Audiometry Treatment: Hearing aid Prophylaxis: ear defenders 4. RIFFLE SHOOTING This usually results in unilateral sensory neural loss, depending on how a person is holding the gun NB: Acoustic trauma’s when sudden very loud noise causes perforation of the eardrum. Sometimes someone can experience if slapped on the ear strongly. There is usually bleeding from the ear. 5. OTOTOXICITY =Drug induced especially by Gentamicin. Caused by medication such as gentamicin which an aminoglycoside 6. Autoimmune associated with SLE, RA 7. Idiopathic hearing los where there is no cause found. 8. AUTOIMMUNE causes like SLE or RA 9. SYNDROMIC HEARING LOSS I. Goldenhar syndrome Either conductive hearing loss or sensory neural hearing loss Associated with skeletal abnormalities like cervical spine or skull. Usually a child Associated with mental retardation or cleft lip or palate II. Alport syndrome Sensory neural hearing loss associated with glomerulonephritis It is progressive in nature. It presents with renal symptoms and hearing loss Family history of Haematuria (Glomerulonephritis) and hearing loss NB: syndromic hearing loss is associated with other abnormalities. 10. NON-SYNDROMIC HEARING LOSS This is when a patient is complaining of hearing loss but actually he/she has no hearing loss or when a patient exaggerate the hearing loss 11. Barotrauma=acoustic trauma: Especially when on flight can lead to perforation of the tympanic membrane. This will cause conductive deafness. 12. Acoustic neuroma=tour of the 8th nerve also called swhanoma. 13. Acute otitis media with effusion will cause conductive hearing loss. 7. VERTIGO Peripheral 1. Meniers disease 2. Benign positional (BPV 3. Vestibular neuritis (labyrinthitis)

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4. Vertebrobasilar insufficiency (artheroscerosis) Drugs due to ototoxicity 1. Gentamicin due to ototoxicity. 2. Diuretics due to postural hypotension 3. Cotrimoxazole 4. Metronidazole Peripheral vertigo usually has severe vertigo + nausea, vomiting + hearing loss + tinnitus + nystagmus (horizontal) While in central vertigo hearing loss and tinnitus are less common 1. Benign positioned vertigo: Sudden onset of dizzines lasting> 30 sec. Exacebated by head movement epecially when turning in bed. Investigation: Dix-Hallpike manoeuvre Px 1. Self-limiting within months 1. Counselling and reassurance 2. Alcohol 3. Betahistine, prochlorperazine 4. Main treatment is manoeuvre called Epley manoeuvre 2. Meniers disease: (DVT) deafness, vertigo and tinitus Also nausea and vomiting

,usually recurent episoes . Intermittent symptoms and

deafness resolves but dizziness persists The main thing is that symptoms occiu in episodes. Treatment:1. Cyclinzine, 2. Prochlorperazine (phenothiazines works by blocking dopamine) 3. Operative decompression of saccus endolyphaticus 3. vestibular neurectomy/ labrynthectomy if persistent. Prophylaxis: betahistamine. 8. VESTIBULAR NEURITIS OR LYBIRINTIS: - Symptoms usually come after viral URTI Sudden vertigo Vomiting The main feature is onset of symptoms after viral ilness. Treatment: cyclinize, improvement occurs in days, full recovery occurs within 2-3 weeks 9. Acoustic Neuroma or verstibular schwanoma: Originates from schwan cell. It is the tumour of the 8th Nerve. It is usually located at the cerebellopontine angle Vestibular schawanoma test S.N- deafness by compressing cochlear N

- Ipsilateral cerebellar signs -

signs

of

reaised

intracranial

pressure

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- Dizziness - Affect other CN 5,6,7,9,10 facial pain or numbness - Usually there is family history. Invx : MRI Treatment: surgery 10. CHRONIC NASAL OBSTRUCTION Child 1. Large adenoids 2. Rhinitis 3. Postnasal space tumour 4. Foreign body Adult: 1. Deflected nasal septum 2. Rhinitis (allergic vasomotor) 3. Polyps 4. Sinusitis 5. Granuloma (TB, sphyllis) 6. Topical vasoconstrictor 1. Vasomotor rhinitis: 1. Bilateral nasal obst. 2. Rhinorrhoea 3. swollen oedematous turbinate’s TREATMENT: No definite Ipratropium nasal spray for Rhinorrhea Cautery or surgery to reduce ^ info turbinate

2. Allergic Rhinitis: 1. May be seasonal (hay fever) or continuous 2. Exposure to allergens like pollens, house dusting 3. Sneezing, pruritis, Rhinorrhoea 4. swollen turbinate’s Px 1. Desensitizing injury 2. Antihistamine 3. Systematic decongestants Epistaxis: This is bleeding from the nose the cause is unknown 80% common in elderly and the commonest cause is hypertension( always check BP)

- More in winter - After trauma (nose picking) - Blood dyscaryosis , alcohol Mx.

Anterior Epistaxis

little’s area

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1. Sitting position, the head downward 2. Apply pressure for 10-15 minutes on soft part if the nose 3. Insert ribbon gauze with xylometazolinet lidocas 4. Cautery with silver nitrate sticks 5. If persists => anterior packing with Vaseline 6. If persistent do posterir packing Posterior Epistaxis 1. If bleeding site is seen
bipolar cautery 2. If cannot be seen
posterior packing 3. If still bleeding
examination under GA + diathermy on ligation of syhenopalati ant. Sinusitis:

1. Fever, facial pain on sinuses which is worse when

you bend forward. 4. Nasal discharge, posterior. Nasal drip 5. Nasal obstruction 6. Anosmia Causes: - bacterial to viral - Swimming in infected water - Septal deviation, polyps (predisposing factors) - Immunodeficiency Investigation: CT scan + rigid endoscopy Treatment: Acute: Bed rest, decongestant, analgesia amoxiclav , if no response
drainage with lavage(washout) STRIDOR 1. Laryngomalacia 2. Laryngitis 3. Epiglotitis 4. Laryngo-tracheo -bronchitis 5. Anaphylaxis 6. Haemangioma, papillomas 7. Trauma (thermal / chemical), intubation Laryngomalacia 1. Present hours after birth 2. Stridor most noticeable in certain position e.g during sleep or when child is excited; 3. Symptoms are worse when child is in lying positing and sympotms improve when child is sat up. Treatment : no treatment need, spontaneous resolution within 2 years is usally the course of the disease. Epiglottitis: 1. Toxic child (child is ill with hugh fever and drooling of saliva) 2. Acute onset 3. Febrile, drooling of saliva 4. Sitting position

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5. Voice muffled 6. Continuous stridor 7. The causative organism is Haemophillus influenza) Rx- do not examine throat, call anaesthetist to intubate the child. - Laryngocopy to see cherry red swollen epiglottis - Blood culture - Cefotaxime Croup: - This is the same as laryngobronchiolitis , it is commoner the epiglottitis - Viral cause (parainfluenza) - Slow onset - Barking cough - No drooling of saliva ( unlike epiglottitis) - Stridor only when child is upset In severe case => cyanosis Treatment: 1. Steroid: dexamethasone oral or budesonide 2. Nebulised adrenaline. 3. Humidified oxygen. HOARSENESS OF VOICE ACUTE 1. Laryngitis this is upper rspiratory tract infection (fever, running nose, sneezing or symply called coryza symptoms) 2. CA larynx (in smokers, elderly patient, weight loss, anaemia, anorexia) 3. Trauma (especially after prolonged intubation) 4. Singing=singer 's nodes 5. Shouting=voice abuse ( e.g peolple after a football match) 6. Laryngeal abscess CHRONIC 1. Laryngitis 2.

Vocal cord paralysis due to recurrent laryngeal N. Palsy

3.

Functional disorders

4. Laryngeal carcinoma. 11. ENT TUMOURS: 1. SINONASAL MALIGNANCY This is a group of malignancy affecting the nose and the sinus system Squamous cell carcinoma account for 70% of all sinonasal tumour Nickel workers are predisposed to SCC (squamous cell carcinoma) Wood workers like carpenters are predisposed to adenocarcinoma Adenocarcinoma accounts for 10% of all tumours LOCATION OF TUMOURS 1. Maxillary 2. Nasal 3. Ethmoid bone

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Symptoms: Nasal obstruction Sinusitis Maxillary symptoms (loose teeth, painful ulcers on the palate, cheek swelling) Ethmoid bone symptoms (diplopia, nasal obstruction, headache) 2. NASOPHARYNGEAL CARCINOMA Symptoms: Epistaxis Nasal obstruction Headache Middle ear effusion NB: everyone presenting with unilateral middle ear effusion must have postnasal space visualisation to exclude tumour Rx: radiotherapy and surgery 3. TONSILLAR TUMOUR 1. The commonest is Squamous Cell Carcinoma (SCC) Common in elderly and middle aged Pain in the throat, otalgia, ulcer on the tonsils, lump in the cheek Investigation: FNAC (biopsy) Rx: surgery with/without radiotherapy 4. LYPHOMA Second commonest tumour Enlarged tonsils Lympadenopathy -Usually there is no mucosa ulceration. (no ulcer on the tonsils) Inx: FNAC (biopsy) Treatment: Radiotherapy

12. OBSTRUCTIVE SLEEP APNOEA This is usually in obese people. They snore a lot during the night and feel tired most of the time during the day. Also they are sleepy during the day. They are usually hypoxic during the night. They wake up very frequently during the night. This condition is also associated with hypertension Investigation: Polysomnography or pulse oxymetry during sleep. 13. COMMON OPERATIONS IN ENT SURGERY 1. TONSILLECTOMY INDICATIONS 1. Recurrent acute tonsillitis 2. Chronic tonsillitis 3. Obstructive sleep apnoea 4. Oral pharyngeal obstruction

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COMPLICATION: Haemorrhage (if between 5-12 days its like infection the cause-this is called secondary haemorrhage. Treat it with antibiotics. Bleeding within 24hrs is called primary haemorrhage (usually its due to bleeding from the operation site) 2. ADENOIDECTOMY INDICATION is adenoids causing obstructive sleep apnoea or adenoid causing glue ear. This condition is usually in children because in adults the tonsils and adenoid they regress. 3.GROMMET INSERTION: Usually done for glue ear 4. ANTRAL WASHOUT: Acute sinusitis not responding to antibiotics in order to obtain microbiology sample

14. FACIAL NERVE PALSY OR 7TH NERVE PALSY CAUSES 1. BELL PALSY: Idiopathic cause of 7 nerve palsy. Excluding other causes makes diagnosis. The commonest cause is a virus. Rx: Prednisolone or simply steroid. Usually there is good recovery within 2 weeks Refer to ophthalmologist due to risk of exposure Keratitis 2. RAMSAY HUNT SYNDROME 7 nerve palsy due to herpes zoster Vesicles in the ear Usually in immunocompromised e.g. diabetes, on steroid, HIV, elderly or cancer. Treatment: Acyclovir oral but if patient immunocompromised then intravenous. 14. TONSILLITIS: Infection of the tonsils Common causes include B-haemolytic streptococcus, pneumococcal, viral. Symptoms: sore throat, fever, enlarged tonsils, white pus or exudates on the throat it means the cause is bacterial and you must treat with antibiotics. Treatment: penicillin V. If patient not able to swallow then admit for intravenous antibiotics Avoid Ampicillin or amoxicillin due to risk of infectious mononucleosis (EBV). If a patient is treated with amoxicillin and the cause was EBV patient may develop rash all over the body. GLANDULAR FEVER =ALSO CALLED INFECTIOUS MONONUCLEOSIS Caused by EBV Symptoms are sore throat with Coryza symptoms Investigation: monospot or Paul bunnel blood test Treatment: analgesia, if you give amoxicillin patient will develop rash all over the body. COMPLICATIONS OF TONSILLITIS: 1. Airway obstruction.

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2. Quinsy: peri-tonsillar abscess. There swelling of the soft palate and the uvula is displaced to one side, drooling of saliva and trismus (failure to open the mouth) Treatment: Incision and drainage 3. Parapharyngeal abscess Diffuse swelling of the neck Admit and do incision and drainage. 15. FOREIGN BODIES (FB) IN ENT FB IN THE EAR Symptoms include: pain in the ear, deafness, or no symptoms. Management: Children need it removed under general anaesthesia Insect use olive oil Soft foreign body e.g. cotton wool use crocodile or Tilley’s forceps Solid FB such as a bead uses a wax hook or probes or sometimes suction. DO NOT USE FORCEPS Refer to ENT if failed attempt or uncooperative child or suspected trauma. FB IN THE NOSE Unilateral purulent foul smelling discharge Nasal obstruction Epistaxis Usually in a child Management: Ask child to blow the nose Solid FB like a bead uses a wax hook or probe Avoid using a pair of forceps as you may push the object forward Soft FB e.g. cotton wool use crocodile forceps or Tilley’s forceps. FB IN THE THROAT ACUTE ONSET OF SYMPTOMS Pricking sensation in the throat Dysphagia Pain in the throat Management: use anaesthetic spray X-ray of the neck Use Tilley’ forceps Refer to endoscope if failed attempt, airway obstruction (urgently) or of good history but can not see FB or if visible FB on X-ray FB OESOPHAGUS IMMEDIATE ONSET OF SYMPTOMS Early presentation Retrosternal pain Drooling of saliva Pain

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Management: X-ray neck and chest Endoscope to remove under GA but if GB below oesophagus expectant management that the FB will pass with stool. Warn patient to come back if FB not passed in 48hrs or sign of intestinal obstruction. NB: sharp objects needs to be removed regardless of the position. NB: sharp objects need to be removed endoscopically as they can cause a cut to the intestines and lead to peritonitis

16. TRAUMA IN ENT FRACTURED NOSE=clinical diagnosis, X-ray not required, refer to ENT for follow if there is a lot of swelling which is making examination difficulty. BASAK SKUL FRACTURE: Rhinorrhhoea or otorrhoea or raccoon eye or battle sign (this is bruises on the mastoid bone) BONES FRACTURED ARE: EITHIMOID BONE (rhinorrhoea or trauma to the forehead) AND TEMPORAL BONE (otorrhoea or fracture to the mastoid) Raccoon eyes =bruises around the eye. Battle sign =mastoid bruising. Resource start date

2013-06-26 09:54

Resource end date

2023-06-27 09:54

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• ◦ ◦ ◦ ◦ • +44 0208 9800 039 +44 0794 0433 068

• • • •

Reports Manager PLAB1-PLAB2 NOTES Administration Sign Out

Resource view Resource name

Epidemiology

Resource description

Epidemiology

Resource content SAMSONPLAB ACADEMY Bow Business Centre Bow Road 153-159 E3 2SE, London Telephone: +44(0)2089800039 Mobile: +447940433068 Email: [email protected]

EPIDEMIOLOGY PLAB 1 NOTES:

Absolute risk of a disease is your risk of developing the disease over a time period. We all have absolute risks of developing various diseases such as heart disease, cancer, stroke, etc. The same absolute risk can be expressed in different ways. For example, say you have a 1 in 10 risk of developing a certain disease in your life. This can also be said to be a 10% risk, or a 0.1 risk - depending if you use percentages or decimals.

Relative risk is used to compare the risk in two different groups of people. For example, the groups could be smokers and non-smokers. Relative risk can either be an increase or a reduced absolute risk. In general, risk factors increase the absolute risk, and treatment reduces the absolute risk. All sorts of groups are compared to others in medical research to see if belonging to a group increases or decreases your risk of developing certain diseases. For example, research has shown that smokers have a higher risk of developing heart disease compared to (relative to) non-smokers.

QUESTIONS: A. In a city in the Bermuda triangle, the absolute risk of developing a disease is 4 in 100 in non-smokers. This risk is increased by 50% in smokers. What is the relative risk of developing a disease in someone who smokes in the Bermuda Triangle? a. b. c. d. e.

10%

1 in 10 2% 6%

1 in 4

Say the absolute risk of developing a disease is 4 in 100 in non-smokers. Say the relative risk of the disease is increased by 50% in smokers. The 50% relates to the 4 - so the absolute increase in the risk is 50% of 4, which is 2. So, the absolute risk of smokers developing this disease is 6 in 100, which is 6%.

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B. In Mozambique, 2 in 20 men develop prostate cancer by the age of 60. New research suggests that taking medication X would reduce the risk of developing this disease by 50%. What is the risk of developing prostate cancer in someone who is taking medication X? a. Relative Risk 10% b. Absolute Risk 10% c. Relative Risk 5% d. Absolute Risk 5% e. Relative Risk 2%

These men have a 2 in 20 risk (which is 10%) of developing prostate cancer by the time they reach the age of 60. Research shows that a new treatment reduces the relative risk of getting this disease by 50%. The 50% is the relative risk reduction, and is referring to the effect on the 2. 50% of 2 is 1. So this means that the absolute risk is reduced from 2 in 20, to 1 in 20 (which is 5%).

NUMBER NEEDED TO TREAT: This is the number of people who need to take the treatment for one person to benefit from the treatment. In Toronto, the absolute risk of developing a myocardial infarction is 4 in 100. A pharmaceutical company reported that medicine X reduced the relative risk of developing this disease by 25%. What is the number needed to treat (NNT)? a. b. c. d. e.

100 50 4 3 1

If the absolute risk of developing the disease was 4 in 100 (which is 4%) then this 25% reduction in relative risk would reduce the absolute risk to 3 in 100 (which is 3%). Therefore, the reduction of the absolute risk after treatment is by 1%. In other words, 100 people need to be treated to save 1 person. SUMMARY: NNT =

100 Absolute Risk Reduction

Absolute risk reduction = Absolute Risk – Relative Risk Absolute risk = the risk of developing a certain disease in a given period of time/life time. Relative risk = an increase in the absolute risk or a decreased absolute risk. i.e. The risk can increase from point A to point R (A = absolute risk, R= relative risk) Treatment can reduce the risk from point A to point R. Therefore: NNT =

100 A - R (Absolute reduction in risk)

EXAMPLE: The absolute risk of developing complications from a certain disease is 4 in 20. Research shows that medicine X reduces the relative risk of getting these complications by 50%. What is the number needed to treat? a. b. c. d. e.

20 10 5 2 1

The absolute risk is reduced from 4 in 20, to 2 in 20. In percentage terms, 4 in 20 is 20%, and, 2 in 20 is 10%. Therefore, the reduction in absolute risk in taking this medicine is from 20% to 10% - a reduction of 10%. The NNT would be 100 divided by 10. That is, 10 people would need to take the medicine for one to benefit. NNT =

100 (20% - 10%)

= 100 10%

= 10

TYPES OF TRIALS: There are many types of studies that explore causal connections. A. Case-control Study:

The frequency of the risk factor (e.g. smoking) is compared between 2 groups, those with the disease (e.g. lung cancer) and those without the disease (control group). This study is retrospective, in that it starts after the onset of the disease. A. Cohort Study:

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The study group consists of subjects exposed to the risk factor (e.g. smoking) and the control group comprises of unexposed people. The incidence of the disease is then compared between the groups over time, prospectively.

BLINDING: If the subject doesn’t know which of the 2 trial treatments he/she is having, this trial is known as single blind. To further reduce the risk of bias, the experimenter should also not know, then this trial is known as double blind. In a good trial, the blind lead the blind.

RANDOMISED CONTROL TRIAL: A study in which a number of similar people are randomly assigned to two (or more) groups to test a specific drug or treatment. One group (the experimental group) receives the treatment being tested, the other (the comparison or control group) receives an alternative treatment, a dummy treatment (placebo) or no treatment at all. The groups are followed up to see how effective the experimental treatment was. Outcomes are measured at specific times and any difference in response between the groups is assessed statistically. This method is also used to reduce bias.

CONFIDENCE INTERVAL: There is always some uncertainty in research. This is because a small group of patients is studied to predict the effects of a treatment on the wider population. The confidence interval is a way of expressing how certain we are about the findings from a study, using statistics. It gives a range of results that is likely to include the 'true' value for the population. The CI is usually stated as '95% CI', which means that the range of values has a 95 in a 100 chance of including the 'true' value. For example, a study may state that 'based on our sample findings, we are 95% certain that the 'true' population blood pressure is not higher than 150 and not lower than 110'. In such a case the 95% CI would be 110 to 150. A wide confidence interval indicates a lack of certainty about the true effect of the test or treatment - often because a small group of patients has been studied. A narrow confidence interval indicates a more precise estimate (for example, if a large number of patients have been studied). CONTROL GROUP: A group of people in a study who do not receive the treatment or test being studied. Instead, they may receive the standard treatment (sometimes called 'usual care') or a dummy treatment (placebo). The results for the control group are compared with those for a group receiving the treatment being tested. The aim is to check for any differences. Ideally, the people in the control group should be as similar as possible to those in the treatment group, to make it as easy as possible to detect any effects due to the treatment.

PLACEBO AND PLACEBO EFFECT: A fake (or dummy) treatment given to participants in the control group of a clinical trial. It is indistinguishable from the actual treatment (which is given to participants in the experimental group). The aim is to determine what effect the experimental treatment has had - over and above any placebo effect caused because someone has received (or thinks they have received) care or attention). RETROSPECTIVE STUDY: A research study that focuses on the past and present. The study examines past exposure to suspected risk factors for the disease or condition. Unlike prospective studies, it does not cover events that occur after the study group is selected. PROSPECTIVE STUDY: A research study in which the health or other characteristic of participants is monitored (or 'followed up') for a period of time, with events recorded as they happen. This contrasts with retrospective studies.

PREVALANCE: Used to describe the proportion of people in a population who have a particular habit, a particular disease or another characteristic. For example, smoking prevalence relates to the proportion of people who smoke in a given population. Prevalence may be expressed in relation to a range of factors including age, sex, socioeconomic and ethnic group. See also incidence.

ABSOLUTE RISK REDUCTION (ARR): A reduction in the likelihood of an event or outcome occurring as a result of a treatment or another intervention. For example, if a treatment reduces the absolute risk of death from 0.25 (25%) to 0.10 (10%), the ARR is 0.15 (15%), that is, 0.25 minus 0.10 equals 0.15. The estimate of absolute risk reduction often comes from clinical trials. The percentage of people taking part who are receiving treatment (treatment group) and experience a specific outcome is compared with the percentage of people taking part but not receiving treatment (control group) who experience the same outcome. MEAN: Mean is the average of a group of values.

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MEDIAN: Median is the middle value when the values are ranked MODE: Mode is the value that occurs most frequently SENSITIVITY: Sensitivity is the proportion of true positives correctly identified by a test SPECIFICITY: Specificity is the proportion of the true negatives correctly identified by the tests.

INCIDENCE: Incidence is the number of new cases divided by the total population per year who are at risk of becoming a case/diseased.

POSITIVITY: • True positive ◦ The individual has the condition and tests positive for the condition ◦ The individual does not satisfy the null hypothesis and the test rejects the null hypothesis

• True negative ◦ The individual does not have the condition and tests negative for the condition ◦ The individual satisfies the null hypothesis and the test accepts the null hypothesis

• False positive ◦ The individual does not have the condition but tests positive for the condition ◦ The individual satisfies the null hypothesis but the test rejects the null hypothesis

• False negative ◦ The individual has the condition but tests negative for the condition ◦ The individual does not satisfy the null hypothesis but the test accepts the null hypothesis

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Genetics

Resource content SAMSONPLAB ACADEMY LIMITED BOW BUSINESS CENTRE BOW ROAD 153-159 E3 SE EMAIL: [email protected] Mobile: 07940433068

GENETICS LECTURE NOTES 2014:

Genetic disease = are those diseases which are inherited from the parents and can be transmitted to the next generation. Genetic counseling is the process by which individuals or relatives are at risk for disorder that may be hereditary are advised of the consequences of the disorder, the probability of transmitting it and ways of in which this may be prevented, avoided or ameliorated. COMMON CHROMOSOMAL DISEASES 1. Down Syndrome • • • •

Chromosomal abnormality, Trisomy 21 Usually present at birth Clinical features (small low set ears, up-slanting eyes, prominent epicanthic folds, flat facial profile, protruding tongue, short neck, mild short stature, short broad hands Associated conditions:

• • • •

Congenital heart disease e.g. VSD< ASD, fallot’s tetralogy Deafness Dementia Cataract Investigation: chromosomal analysis showing additional chromosome 21 Management: Patient needs cardiac investigations and testing for hearing.

1. Klinefelter’s syndrome

• Boys with klinefelter syndrome enter puberty normally but by mid puberty the testes become small • Infertility due to azoospermia, Gynaecomastia. They have decreased testosterone.

Investigation: Chromosomal analysis. Test to prove the azospermia is testosterone.

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1. Patau syndrome

• Trisomy 13 • Microcephaly, Microphthalmia • Cleft lip and palate

Investigation: chromosomal analysis 1. Edwards Syndrome:

• • • • •

Trisomy 18 Features: Congenital heart disease Low birth weight Overriding fingers Usually they die within 4 days. Rarely they can live several months.

1. Turner’s syndrome

• Most girls have single chromosomal (45, XO) • Features: Short stature, broad neck, ptosis, widely spaced nipples, congenital heart disease,

GENETIC DISORDERS WITH CARDIAC FEATURES 1. Marfan syndrome

• Autosomal dominant multisystem disorders caused by mutation in the in the chromosome 15. • Features: Include, tall and slim body build with long limbs scoliosis, long fingers, aortic aneurysm

1. Di George syndrome

• Short stature • Congenital heart abnormality e.g. tetrology fallot • Prominent nasal bridge

1. Williams syndrome

• Autosomal dominant • Peri-orbital fullness, short stature, congenital heart abnormality chest deformity.

GENETIC DISORDERS WITH LEARNING DISABILITY

1. Fragile X syndrome

• • • •

It is commonest inherited disease of mental retardation Boys with Fragile X syndrome usually have global developmental delay Can affect both girls and boys They boys have stereotyped repetitive behavior such as hand flapping and resistance to change of routine.

1. Prader-Willi Syndrome

• Babies are frail and may fail to thrive • Older children have learning difficulty and short stature.

Genetic disorders with neuromuscular features: 1. Congenital Myotonic Dystrophy

• It is an autosomal dominant with onset usually in adult life • At birth the baby is floppy • During pregnancy there is polyhydrominous

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• Usually the affected children are from women who are also have myotonic dystrophy

1. Duchene muscular dystrophy

• • • • •

Presents with development delay Child climb up his thigh when standing up (Gower’s sign) Diagnosis is by genetic testing X-linked recessive Mean age of onset is 5 years.

1. Spinal muscular atrophy

• Autosomal recessive disorders • Symmetrical proximal weakness as a consequence of degeneration of anterior horn cells of spinal cord

Investigation: genetic molecular testing GENETIC DISORDERS WITH DERMATOLOGICAL FEATURES

1. Ehlers Danlos syndrome

• Autosomal dominant • Hypermobility of small and large joint with soft skin • Soft skin which hyper-extensive

1. Neurofibromatosis

• • • •

NF1 has a autosomal dominant disease Café au lait spots Neurofibroma Chance of transmitting it to children is 1:2

1. X-linked hypohydrotic ectodermal dysplasia

• It is X linked recessive • Boys have reduced sweating which may cause dangerous hyperpyrexia in infancy

1. Tuberous sclerosis

• Autosomal dominant • Characterized by hamartoma’s on the skin, brain and other organs • Commonly presents with infantile spasm, seizures and mental retardation

OTHER INHERITED DISEASES 1. Polycystic kidney disease:

An autosomal dominant disease is associated with vascular abnormality like berry aneurysm. The kidney is usually palpable bilaterally and patient has hypertension. 1. Cystic fibrosis:

This is an autosomal recessive disease: meaning there is 1:4 chance of transmitting to another child. Child presents with failure to thrive and pancreatic insufficiency and recurrent chest infection. Investigation: sweat test 1. Glycogen storage disease:

Specific enzyme defects preventing mobilization of glucose from glycogen and resulting in abnormal storage in liver and muscle. Patient usually presents with hypoglycemia in the morning. This is autosomal recessive condition usually presenting with hypoglycemia, lactic acidosis, poor growth, mental retardation. 1. Haemophilia:

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This is a X-linked recessive disease affecting male children and presents with bleeding into the muscles and joints. 1. Achondrioplasia:

Short limbs, autosomal dominant lumbar lordosis, large head. 1. Von Willebrand’s:

An autosomal dominant disease causes high bleeding time and bruises and bleeding. POLYGENIC INHERITANCE DISEASE: These are disease which can run in the family but there needs to be interaction with external environment which include the following: A. Diabetes B. Multiple sclerosis

AUTOSOMAL RECESSIVE DISEASES: 1. Sickle Cell Disease 2. Thalassemia 3. Cystic Fibrosis

AUTOSOMAL DOMINANT DISEASES:

1. 2. 3. 4.

Polycystic Kidney Disease Huntington Disease Neurofibromatosis Von Willibrand Disease X-LINKED DISEASES:

1. Duchene Muscular Dystrophy 2. Haemophilia

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SAMSONPLAB ACADEMY Bow Business Centre Bow Road 153-159 E3 2SE, London Telephone: +44(0)2089800039 Mobile: +447940433068 Email: [email protected]

GASTRO- ENTEROLOGY OVERVIEW OF TOPICS

1. Dysphagia 2. Dyspepsia 3. Peptic Ulcer 4. Zollinger Ellison Syndrome 5. Gastro-oesophageal reflux disease 6. Inflammatory Bowel Disease 7. Irritable Bowel Syndrome 8. Coeliac Disease 9. Jaundice & Liver Diseases 10. Primary Biliary Sclerosis 11. Primary Biliary Cirrhosis 12. Sclerosing Cholangitis

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13. Primary Sclerosing Cholangitis 14. Alpha 1- antitrypsin deficiency 15. Hereditary Haemochromatosis 16. Pancreatic Diseases 17. Pancreatitis 18. Pancreatic Cancer 19. Diarrhoea 20. Constipation 21. Colorectal Carcinoma

A. DYSPHAGIA SIGNS & SYMPTOMS

INVESTIGATION MANAGEMENT

Progressive dysphagia (dysphagia of solids then liquids), old age , weight loss, anemia ( pallor, fatigue, palpitations), anorexia

1. Barium swallow (initial investigation) 2. Endoscopy & biopsy as definitive diagnosis

Surgery resection if no metastasis

ACHALASIA Pathology in myenteric pleuxs. Failure of the lower oesophageal sphincter to relax, due to decreased in ganglion cells in the oesophageal wall

Dysphagia of both fluids and solids Regurgitation Weight loss

Barium swallow

Dilatation or Heller’s myotomy

DIFFUSE OESOPHAGEAL SPASM –abnormal oesophageal motility

Intermittent dysphagia +/chest pain due to reflux which may happen with this condition

Barium swallow

Dilatation

SCLERODERMA – replacement of the smooth surface with fibrosis leading to decreased oesophageal sphincter function

Reflux

PHARYNGEAL POUCH

Regurgitation of undigested food Sensation of lump in the throat Halitosis Bulging of neck on drinking Aspiration into lungs

If presents as dysphagia à Barium swallow

Surgical excision

If child then while playing

Barium swallow

CAUSES

OESOPHAGEAL CANCER

FOREIGN BODY

Radiotherapy if with metastasis

If presents as neck mass à ultrasound scan

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with toys & usually child is normal & healthy.

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Removal of the foreign body by endoscopy

If adults then during eating chips, meat, fish etc.

OESOPHAGEAL STRICTURE

Due to ingestion of corrosives e.g. acid and due to GERD

MOTOR NEURONE DISEASE (Bulbar palsy)

Dysphagia + weakness of the lower limbs, usually male patient, middle aged, no sensory loss / no sphincter abnormalities, eye muscles not affected

PLUMMER VINSON SYNDROME/ PATERSON BROWN KELLY SYNDROME – there is post – cricoid web. This is due to spasm of upper oesophageal sphincter

Iron deficiency anaemia usually female patient, koilonychia

LOWER OESOPHAGEAL RING: Schazki ring

Narrowing of the lower end of the oesophageal sphincter, the mucosa forms a ring

STROKE

Sudden + symptoms like hemiplegia, visual defects, usually in old patients

GLOBUS HYSTERICUS

Feels lump in the throat which need to be swallowed. Associated with anxiety, this can be complication of GERD.

OESOPHAGEAL CANDIDA

White plaques or ulceration in the mouth, in immunecompromised patient e.g. HIV

Dilatation of the stricture

Treating anaemia by iron tablets

Reassurance Barium swallow

CT scan

Anti – fungal (fluconazole)

OESOPHAGITIS

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Complication of GERD with symptoms of reflux MYASTHENIA GRAVIS

Dysphagia + other symptoms like diplopia, fatigue by the end of the day, weakness of the eye muscles, tiredness + diplopia at the end of the day, Fatigue + dysphagia

CHAGAS DISEASE

After many years of the disease can cause dilatation of the oesophagus (mega – oesophagus) leading to dysphagia

EXTRINSIC PRESSURE (LUNG CANCER), RETROSTERNAL GOITRE, AORTIC ANEURYSUM, LEFT ATRIUM ENLARGEMENT

General symptoms of cancer Symptoms of thyroid Different blood pressure in each arm, pain radiating to the back History of mitral valve disease

PARKINSONISM

Shuffling gait Dizziness Ataxia Nystagmus, resting tremors, cog wheel/lead pipe rigidity

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PPI or H2 antagonist

Treating the cause

DYSPEPSIA This is epigastric pain or discomfort with or without nausea and vomiting.

ALARMS 55 A - Anorexia L - Loss of weight A - Anaemia R - Recent onset of progressive symptoms M - Melena or haematemesis S - Swallowing difficulties 55 - Patient 55 or more years old

STEPS OF MANAGEMENT FOR NEW DYSPEPSIA

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1. If age > 55 years or ALARM Signs present then perform urgent endoscopy. 2. If age < 55 years and no ALARM Signs then

Treat with lifestyle modifications, simple antacids +/- anti-reflux for 4 weeks. • If symptoms resolve then no further action required. • If symptoms persist then do test for H.Pylori.

1. If H. Pylori test is positive then eradicate H. Pylori and review after 4 weeks. • If symptoms resolve then no further action required. • If symptoms persist then do a urea breath test. • If this is positive then continue H. Pylori eradication. • If this is negative then consider UGI endoscopy.

1. If H. Pylori test negative then give PPI’s or H2 blockers x 4 weeks e.g. Omeprazole 20 mg/24hrs or

Ranitidine 150 mg/12 hrs. • If there is improvement then no further action required. • If there is no improvement then give longer term, low dose treatment of the same medications and consider UGI

endoscopy. Triple therapy for eradication of Helicobacter pylori: 1. PPI 2. Clarithromycin 3. Amoxicillin or Metronidazole DIFFERENTIAL DIAGNOSIS 1. Peptic ulcer 2. GERD 3. Mallory-Weiss tear 4. Oesophagitis 5. Gastric carcinoma 6. Gastric erosions due to (NSAIDS, steroids, gastrinoma)

PEPTIC ULCER • Gastric ulcer: Patients usually present with epigastric pain after meals +/- relieved by antacids, patients usually lose

weight due to fear of pain when they eat. • Duodenal ulcer: Patients usually experience pain at night or before a meal. They are also called hunger ulcers.

Pathogenesis of Peptic Ulcer:

Aggravating Factors Helicobacter pylori HCI Pepsin

Protective Factors HCO3 Mucus Prostaglandins

Investigations in Peptic Ulcer Disease: H. pylori test can be performed with different techniques: 1. Urea Breath Test a. Pre-treatment test (before performing endoscopy): best test option is the carbon-13 urea breath

test or stool antigen test for H. pylori. b. Post – eradication testing: best performed using carbon-13 urea breath test

N.B: Before performing H. pylori test, stop PPI and antibiotics to reduce the chance of false positive.

1. Endoscopy – gold standard investigation but not practical to be done in all patients. a. Done to visualize ulcers which are usually clean and smooth with sharp margin b. Has the benefit of taking biopsy for suspicious lesions and test for H. pylori

1. Barium studies – may be used if patient is refusing endoscopy.

Zollinger – Ellison Syndrome

• It is due to a gastrinoma in the pancreas which causes increased HCl leading to multiple ulcers in the stomach,

duodenum & small intestines (it’s an unusual ulcer and doesn’t respond to antacids) • About 20 - 25 % of gastrinoma patient have MEN-1 syndrome

Investigations: High fasting serum gastrin or pancreas tumour

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Management: • Medical therapy → Proton Pump Inhibitor • Surgical therapy → Removal of tumours

Gastro-oesophageal reflux disease:

• Dysfunction of the lower oesophageal sphincter predisposes to the reflux of acid from the stomach to the oesophagus • Associated with smoking, obesity, alcohol, rolling/sliding hiatus hernia – displacement of the part of the stomach into the

thorax (rolling hernia can cause strangulation), pregnancy, obesity, big meal Investigations: endoscopic or clinical diagnosis Endoscopic evidence: Oesophagitis Clinical evidence: Heart burn There are two types of symptoms: Typical and Atypical Typical symptoms 1. Heartburn/ retrosternal burning or discomfort related to meals or lying down therefore pain at night, pain is relieved by

antacids 2. Water brush = excessive salivation 3. Odynophagia (painful swallowing) if there is oesophagitis

Atypical symptoms 1. Globus hystericus 2. Recurrent pneumonitis 3. Angina like chest pain

Complications: • Oesophagitis • Oesophageal stricture • Barrett’s oesophagus/CLO (Columnar line oesophagus) - transformation of squamous cells into columnar cells in the

oesophagus, pre- malignant stage – needs regular endoscope surveillance • Oesophageal adenocarcinoma

Medication: 1. Simple antacids (Magnesium Trisilicate) 2. If oesophagitis confirmed → Proton Pump Inhibitor 3. Prokinetics like metoclopramide, they help emptying of the stomach if there is gastric paresis

Main Points In Managing GERD 1. If age > 55 years or ALARM Signs present then perform Urgent endoscopy

1. If age < 55 years and no ALARM Signs then lifestyle modifications plus antacids for 4 weeks are the first line steps of

management in patient with typical GERD symptoms. Eg. • Lose weight • Stop smoking • Small regular meals • Raise the head end of the bed • Avoid hot drinks, alcohol • Avoid eating < 3 hours before bed

1. If lifestyle modifications not helpful, offer Proton Pump Inhibitor for 4 weeks. • If symptoms resolve then no further action • If symptoms persist, perform an endoscopy A. If endoscopy is positive ie. shows oesophagitis then prescribe PPI/H2 antagonist • If symptoms resolve with PPI/H2 antagonist then no further action • If symptoms persist even with PPI/H2 antagonist then perform Fundoplication

A. If endoscopy is negative (ie. normal) then do 24 hour pH monitoring • If 24 hour pH monitoring is +ve prescribe PPI/H2 antagonist (if symptoms persist even with PPI, do fundoplication) • If 24 hour pH monitoring is –ve then check for alternative diagnosis 1. If symptoms persist after fundoplication, do endoscopy first and then pH monitoring (if required) to check if there is still

ongoing reflux.

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INFLAMMATORY BOWEL DISEASE

Associations

Ulcerative Colitis

Crohn’s Disease

Affects mucosa and sub-mucosa, Formation of ulcers Mucosa is friable and bleed easily No skip lesions Rectosigmoid is commonly involved with 50% Never spreads proximally to the ileocaecal valve Common in NON SMOKERS

Affects mouth to anus Transmural inflammation Granulomatous lesion Terminal ileum is 50% Skip lesions with rectal sparing (usually) Cobblestone ulceration as a result of aphthous ulceration progression to oedema and nodular thickening Rose thorn appearance Associated with smoking & low fibre diet intake

Gradual onset Chronic diarrhea with blood & mucus ¯ weight Urgency & tenesmus occur with rectal disease Extra-intestinal symptoms are clubbing, aphthous ulcers, erythema nodosum, pyoderma gangrenosum, conjunctivitis, arthritis, ankylosing spondylitis, cholangio-carcinoma Associated with primary sclerosing cholangitis

Chronic diarrhea ¯ weight Aphthous ulcer Abdominal tenderness Right iliac fossa pain Perianal abscess / fistula / skin tags Fistulas elsewhere Granulomata Strictures and ulcers SAME extra intestinal symptoms as UC

Investigations

Sigmoidoscopy – granular inflammation, ulcers, crypt abscesses

Sigmoidoscopy Barium enema Colonoscopy + Biopsy

Treatment

Mild: < 4 motion/day & patient is well = prednisolone + mesalazine (amino salicylates) Moderate: 4-6 motion/day & patient is well = oral prednisolone + mesalazine + twice daily steroid enema Severe: IV hydrocortisone + twice daily enemas

Mild: prednisolone Severe: hydrocortisone + metronidazole

Signs & Symptoms

The role of aminosalicylates is prevention of relapse in Crohn’s is less effective than in UC

Prevention of relapse: aminosalicylates (mesalazine, sulphasalazine)

Complications

1. Perforation - do erect Chest X-Ray 2. Colonic carcinoma - risk is 15% 3. Toxic megacolon (dilatation of colon) can lead to perforation

IRRITABLE BOWEL SYNDROME:

Group of abdominal symptoms with “NO ORGANIC CAUSE” which can be found.

Signs & Symptoms: • Patient is usually 20 – 40 years old • Central abdominal pain relieved by defecation • Abdominal bloating • Altered bowel habits < constipation alternating with diarrhoea • Chronic > 6 months • Exacerbated by stress or eating

Investigations: all investigations and examinations are normal therefore it is diagnosis by exclusion NB. Clues to rule out other causes: • No weight loss • No bleeding

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• No night symptoms i.e. diarrhoea or abdominal pain at night • All investigations are normal

Treatment: Symptomatic e.g. for pain mebeverine hydrochloride (anti- spasmodics)

COELIAC DISEASE

This is a T – cell mediated autoimmune disease of the small bowel in which protamine causes villous atrophy and malabsorption Signs & Symptoms: • • • • •

Steatorrhoea Abdominal pain Weight loss / failure to thrive in children Weakness Folic acid or iron deficiency anaemia

Investigations: Antibodies • Anti - endomyseal • Anti -

α gliadin

• Anti – transglutaminase • Ig A anti body duodenal biopsy

Treatment: Life long gluten free diet

Complications: 1. 2. 3. 4. 5.

Iron deficiency anaemia Folate deficiency anaemia Osteoporosis Lymphoma Secondary lactose intolerance

JAUNDICE & LIVER DISEASES General Approach A: OBSTRUCTIVE JAUNDICE: ALP and/or GGT is higher than AST and ALT. Bilirubin is high as well. B. HEPATIC PICTURE: ALT and/or AST raised higher than ALP or GGT. Bilirubin is high as well. C. ISOLATED RISE IN BILIRUBIN: Unconjugated bilirubin: Hemolysis, Gilbert syndrome (congenital disease) Conjugated bilirubin: Dubin -Johnson syndrome (congenital disease) D. ISOLATED RISE IN GGT: Suggests alcohol abuse E. ISOLATED RISE IN ALP: Usually not due to liver disease but to a bone disease like bony metastasis, Paget’s disease, osteomalacia

1. PRE-HEPATIC JAUNDICE Causes: • Hereditary haemolytic anaemia • Acquired haemolytic anaemia, malaria

Signs & Symptoms: anaemia + jaundice

Investigations: 1.↑ unconjugated serum bilirubin 2. Evidence of haemolysis: ↓haemoglobin,↑reticulocylosis 3. 4.

↓haptoglobin ⊥ FT (N)

2. HEPATIC JAUNDICE Causes: a. VIRAL HEPATITIS A,B,C,D,E - If acute → A, E ( Faeco - oral route) - If chronic → B, C, D (Body – fluids) Risk Factors for Hepatitis B & C: IV drug abuser, Blood transfusion, Homosexual

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b. ALCOHOL HEPATITIS Strong history of alcohol drinking Sign’s: presence of spider naevi + stigmata of chronic liver disease, ↑GGT c. DRUG INDUCED – eg. paracetemol d. GILBERT’S SYNDROME - impaired conjugation

3. POST – HEPATIC JAUNDICE (OBSTRUCTIVE JAUNDICE) Causes: 1. Common bile duct stones 2. Tumours of head of pancreas

→ Courvoisier’s sign (presence of palpable painless gall bladder + jaundice unlikely due

to gallstones) 3. Primary biliary cirrhosis 4. Primary biliary sclerosis 5. Sclerosing cholangitis 6. Primary Sclerosing Cholangitis 7. Alpha 1 –Antitrypsin Deficiency 8. Hereditary haemochromatosis

Signs & Symptoms: • Pale stools + dark urine • ↑ Serum conjugated bilirubin • No urobilinogen in urine • ↑↑ Alkaline phosphatase

PRIMARY BILIARY CIRRHOSIS Chronic inflammation of autoimmune origin which leads to destruction of interlobular bile ducts in the liver causing progressive cholestasis, cirrhosis & portal hypertension

Signs & Symptoms: It is usually asymptomatic but can have the following symptoms: 1. Pruritis - causing scratch marks on the body 2. Jaundice 3. Skin pigmentation which is progressive in nature & starts in an early age 4. Hepatomegaly 5. Splenomegaly 6. Osteoporosis 7. Usually young female patients

Investigations: 1. ↑ALP,↑GGT & mildly raised AST AND ALT 2. Ultrasound scan to rule out bile stones 3. Anti-mitochondrial antibodies

Treatment: Cholestyramine for pruritis Urodeoxy - cholic acid improves cholestasis

PRIMARY SCLEROSING CHOLANGITIS: Cause unknown, there is an immunological theory, there is fibrosis & stricture of the intra & extra hepatic bile ducts. Signs & Symptoms: Pruritus with or without fatigue. In advanced cases there may be ascending cholangitis, cirrhosis and end-stage hepatic failure Investigations: •

↑ ALP

• ERCP shows multiple strictures

Treatment: • Liver transplant is the mainstay for end-stage disease • Cholestyramine for pruritus • Ursodeoxy – cholic acid • Antibiotics if there is cholangitis • Endoscopic stenting helps relieve strictures • Yearly ultrasound scans to check for cholangiocarcinoma

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Complications: Cancer may occur in the bile duct and gall bladder. Cancer of the liver and colon cancer are more common. Monitoring: Regular LFT, ultrasound and AFP. It is also advisable to perform yearly colonoscopy.

α 1 –ANTITRYPSIN DEFICIENCY The glycoprotein α1 – anti trypsin is one of the family of serine protease inhibitors. 1. The defect means it cannot be released from the liver where it synthesized, therefore accumulation leads to liver

disease as a child. 2. Its function is to oppose protease therefore without it protease activity is unopposed and it causes to destruction of the

alveoli leading to emphysema as an adult. Investigation: • ↓ serum anti-trypsin level • Liver biopsy

Treatment: Supportive

HEREDITARY HAEMOCHROMATOSIS: This is an inherited disorder of iron metabolism in which there is ↑ intestinal iron absorption, which tends to deposition in all organs

Signs & Symptoms: Asymptomatic in early stages then leads to 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13.

Weakness Fatigue Joint pains Abdominal pain Arthralgia Grey/bronze skin pigmentation Diabetes mellitus Erectile dysfunction Signs of chronic liver disease Hepatomegaly Cirrhosis Cardiomyopathy Neurological or psychiatric symptoms

Investigations: • •

↑ LFT ↑serum ferritin ↑ serum iron

• • Joint x-ray = chondrocalcinosis

Treatment: Venesection every week to every two weeks Complications:

↑ risk of hepatocellular carcinoma due to high ferritin Hemosiderin

HEPATOCELLULAR CARCINOMA The commonest (90%) liver tumours are secondary (metastatic) tumours eg. from breast cancer, bronchial cancer, GI tract cancers. Strongly associated with liver cirrhosis High risk factors • • • •

Family history Hepatitis B and C Inherited haemochromotosis (high ferritin) Primary biliary cirrhosis

Signs and Symptoms • • • • • •

Fever and malaise Anorexia, weight loss Right upper quadrant pain Hepatomegaly Jaundice Ascites

Investigations: • CT scan is the investigation of choice • AFP (Alpha-fetoprotein) is high

Treatment: 1. Surgical resection if there is a single lesion and no liver metastasis 2. Liver transplant gives 5 years survival rate

Prevention: Hepatitis B vaccination PANCREATIC DISEASES

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1. ACUTE PANCREATITIS Causes can be remembered as GET SMASHED: 1. 2. 3. 4. 5. 6. 7. 8. 9. 10.

Gallstones Ethanol Trauma Steroids Mumps Autoimmune Scorpion sting Hyperlipidemia/ Haemochromatosis ERCP Drugs

Signs & Symptoms: • Severe epigastric pain which radiates to the back relieved by sitting forward • Often precipitated by recent alcohol abuse • Acute: Acute generalized tenderness with symptoms of peritonitis and paralytic ileum • Chronic: weight loss, steatorrhoea (↑ fat content in the stool) causing pale foul smelling stools, difficult to flush.

GLASGOW CRITERIA FOR PREDICTING SEVERITY OF PANCREATITIS • • • • • • • •

PaO2 < 8kpa (do ABG) Age > 55 years Neutrophil WCC > 15 x 10*9 Calcium < 2 mmol/L Renal function Urea > 16 mmol/L Enzymes LDH >600 IU/L, AST >200 IU/L Albumin 10 mmol/L

Investigations: 1. Investigation of choice is serum amylase to confirm diagnosis 2. Plasma lipase can also be used and is more sensitive than amylase 3. Ultrasound scan to look for gallstones 4. CT abdomen is the gold standard if diagnosis is not clear after checking amylase and lipase

Treatment: 1. IV fluids and Nasogastric tube if vomiting 2. Prophylactic antibiotics 3. Gallstone-related pancreatitis needs urgent ERCP and laparoscopic cholecystectomy should be performed

within 2 weeks.

1. PANCREATITIC CANCER It is common in elderly patients and usually causes painless obstructive jaundice. Risk Factors: 1. Smoking 2. Chronic pancreatitis 3. Diabetes Mellitus 4. Family history of pancreatic cancer

Signs & Symptoms: • Head of the pancreas tumours usually cause obstructive jaundice whereas tumours of the tail of the pancreas cause

obstruction of the inferior vena cava. • Weight loss • Anorexia • Abdominal pain • Jaundice • Back pain • Migrating thrombophlebitis • Courvoiser’s signs – distended non tender palpable gall bladder

Investigations: 1. Abdominal ultrasound is the initial investigation 2. CT scan is the gold standard but is only indicated in patients with highly suspicious signs of pancreatic

tumour 3. Serum marker: CA 19-9 4. ERCP: indicated when other modalities are inconclusive and suspicion of malignancy is still high. May be

used to take biopsy and insert a stent at the same time. 5. Biopsy: should be done during endoscopic procedure.

Treatment:

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1. Resection with intent to cure: for patients with localized tumours and fit enough to tolerate major surgery

(e.g. whipple’s procedure) 2. Palliative therapy: if there is metastasis

DIARRHOEA

This is increased frequency of defaecation and watery or loose stools.

ACUTE DIARRHOEA: 2 WEEKS Causes: 1. Colorectal cancer: altered bowel habits, weight loss, blood in stools, anaemia 2. Irritable Bowel Syndrome: chronic diarrhoea alternating with constipation, pain relieved on defecation, no other

pathology 3. Diabetic Autonomic Neuropathy 4. Hyperthyroidism 5. Addison’s Disease 6. Carcinoid syndrome

CAUSES OF BLOODY DIARRHOEA: 1. E-coli 2. Camphylobacter 3. Shigella 4. Salmonella 5. Amoebiosis 6. Cronh’s 7. Colorectal Cancer 8. Polyps 9. Ischaemic colitis 10. Pseudomembranous colitis • Travel history present → E-coli, Camphylobacter, Shigella, Salmonella, Amoebiasis • History of long term antibiotics can cause Pseudomembranous colitis (caused by Clostridium difficile) • History of Myocardial Infarction/Intermittent claudication → Mesenteric ischaemia (s&s = post prandial pain) • Tenesmus→ Suggests rectal involvement

Treatment: • Oral Rehydration • Loperamide

CONSTIPATION Pass stool < 3 times per week Clinical Features: • • • • • •

A mass can be felt inside the rectum due to faecal impaction Sigmoid colon may be palpable Typically in elderly & children May present with confusion in elderly May also present with overflow diarrhoea Usually constipation leads to faecal impaction causing obstruction of the urinary tract leading to UTI which may cause confusion in the elderly

Management: • Life style modifications (advise exercise/high fibre diet /high fluid intake) • If the above fails then give medications

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1. Bulking Agents e.g. Methylcellulose, Ispaghula

They ↑ faecal mass, therefore stimulating peristalsis. They must be taken with plenty of fluids & they take days to act. Contraindications: Intestinal obstruction Colonic atony Faecal impaction 1. Stimulant Laxatives e.g. Bisacodyl, Senna – these are tablets, Glycerol – acts like a stimulant, used as

rectal suppository They increase intestinal motility. Contraindications: Intestinal obstruction Acute colitis (fever + diarrhoea with blood) NB. Stimulant laxatives are the first choice when treating constipation caused by opiates 1. Faecal Softeners e.g. Arachis oil – as an enema, Liquid paraffin (should not be used for prolonged period)

Lubricates & softens stools, very useful when managing constipation with anal fissures. 1. Osmotic Laxatives e.g. Lactulose

They retain fluid in the bowel. Contraindication: Intestinal obstruction 1. Enemas: Useful when there is a need of rapid evacuation of stony dull faecal impaction, manual

evacuation may be performed

COLORECTAL CARCINOMA Risk factors • Age • Smoking • Polyps • Inflammatory Bowel Disease • Low fibre diet • Family History • Familial Adenomatosis Polyposis • Diabetes Mellitus Type 2

NB. Most cancer develops from polyps in the colon, which developed at least a decade before the cancer develops Presentation 1. RECTAL CANCER • Fresh bleeding per rectum • Sensation of incomplete evacuation • Tenesmus • Painful defecation • Weight loss

1. COLONIC CANCER ◦ RIGHT COLON TUMOURS ◾ Usually become fairly large before any obstructive symptoms occur ◾ Change in bowel habits it usually a late sign ◾ Patients usually present with iron deficiency anaemia ◾ Crampy abdominal pain intermittently

◦ TRANSVERSE AND LEFT COLON TUMOURS ◾ Iron deficiency anaemia is uncommon ◾ Commonly present with intermittent rectal bleed ◾ Crampy abdominal pain intermittently

Investigations: • Rectal Cancer → sigmoidoscopy • Sigmoid colon Cancer → sigmoidoscopy • Colonic Cancer → colonoscopy

N.B: CEA is a colorectal tumour marker Treatment: Surgery Resource start date

2013-06-30 06:13

Resource end date

2023-07-01 06:13

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• ◦ ◦ ◦ ◦ • +44 0208 9800 039 +44 0794 0433 068 • • • •

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SAMSONPLAB ACADEMY Bow Business Centre Bow Road 153-159 E3 2SE, London Telephone: +44(0)2089800039 Mobile: +447940433068 Email: [email protected]

HAEMATOLOGY LECTURE NOTES 2014 TOPICS:

1. Anaemia 2. Microcytic Anaemia 3. Iron Deficiency Anaemia 4. Thalassemia 5. Normocytic Anaemia 6. Congenital Spherocytosis 7. Glucose-6-phosphate Dehydrogenase Deficiency 8. Sickle Cell Disease 9. Autoimmune Haemolytic Anaemia 10. Macrocytic Anaemia 11. Pernicious Anaemia 12. Bleeding Disorders 13. Abnormal Coagulation 14. Haemophilia A 15. Haemophilia B 16. Anti-coagulant Therapy 17. Bleeding in liver disease 18. Massive transfusion/cardiopulmonary bypass 19. Abnormal Platelets 20. Thrombocytopenia (ITP) 21. Vascular Defect 22. Malignancies in Haematology

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23. Pancytopenia 24. Leukaemias 25. Acute Lymphoid Leukaemia 26. Acute Myeloid Leukaemia 27. Chronic Myeloid Leukaemia 28. Chronic Lymphoid Leukaemia 29. Hodgkin’s Lymphoma 30. Non-Hodgkin’s Lymphoma 31. Myeloma 32. Myeloproliferative Disorders 33. Polycythemia Rubra Vera 34. Essential Thrombocytopenia

ANAEMIA This is low haemoglobin levels. Parameters for anaemia: Hb 60 years, ESR ↑, back pain, anaemia and high ESR)

GLUCOSURIA Usually due to diabetes mellitus, there might be ketones in the urine as well.

↑ WHITE CELL COUNT Usually due to infection.

KETONES Usually in diabetic ketoacidosis, starvation or dehydration. There might be glucosusia.

NITRATE A sign of infection, the commonest causes are E.coli, Proteus and Klebsiella. So there will be fever.

MICROSCOPY OF MID-STREAM URINE: 1. ↑ Leukocytes: common cause is urinary tract infection 2. ↑ Red cells: means haematuria 3. Casts: these are cylindrical aggregates formed in the distal tubules or collecting ducts. There are different types:

a. b. c. d. e.

Hyaline casts and fine granular casts are normal findings. Hyaline casts are mainly protein. Red cell casts indicate glomerulus bleeding, usually due to glomerulonephritis. White cell casts suggest acute infection, usually bacterial (pyelonephritis). Fatty casts can occur in nephrotic syndrome. Tubular cell casts occur in acute tubular necrosis (ATN).

4. Crystals: OXALATE - indicate predisposition to form calculi CYSTINE - diagnostic of cystinuria 5. Glomerular Filtration Rate: Normal is 120 ml/min, if it falls below 30 ml/min then it causes urea and creatinine to accumulate in the body. High levels of creatinine indicates renal failure. 6. Immunological Investigation:

a. Anti-Neutrophil Cytoplasmic Antibodies (ANCA) - suggests vasculitis b. Anti-Glomerular Basement Membrane Antibodies - suggest Goodpasture's Syndrome. c. Anti-Nuclear antibodies and Double Stranded DNA for antibodies and low Complement levels -suggests SLE. 7. Ultrasound Scan: Good for evaluation of renal masses, hydronephrosis and for any renal masses e.g. tumour or polycystic kidney disease. 8. KUB (x-ray Kidney Ureter and Bladder): the initial investigation for all renal stones and it can detect 99% of all radiolucent stones. Radio-opaque stones like urate stones are not visible on KUB. 9. Intravenous Urography (IVU) or Excretory Urograph: the investigastion of choice for all renal stones. 10. Renal Biopsy: is used for chronic and acute renal failure, nephrotic syndrome and glomerulonephritis if the cause is not known. 11. Retrograde Pyelography: is used to determine the lower level of obstruction after IVU or ultrasound scan has shown obstruction. 12. Cystoscopy: is the investigation of choice in bladdar tumour.

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13. CT KUB: can be used instead of IVU for evaluation of renal stones. NICE guidelines recommend IVU. So if you have both of them in the options choose IVU. 14. Antegrade Pyelography: Percutaneous injection of contract into the pelvi-calyceal system and ureter. It is used when ultrasound scan has shown dilated pelvi-calyceal system in a patient with suspected obstruction. It is used when a draining catheter is need to be placed i.e nephrostomy. Also, if a stent needs to be put if there is a Ureter Stricture. 15. Micturating Cystourethrography (MCU): This investigation is done to look for vesicoureteric reflux, It is an investigation which is done in children only to look for vesicoureter reflux. If reflux is found in children surgery is usually done. 16. Renal Arteriography: is used in renal artery stenosis 17. Dynamic Scintigraphy: Uses Technium 99 (Tc99). Contrast is inserted into the veins and it is followed by a gamma camera. It allows to detect renal perfusion e.g. in renal stenosis. Indications:

a. Renal artery stenosis is suspected as a cause of high blood pressure. b. In severe oliguria e.g. post-trauma, post aortic surgery or after kidney transplant. 18. Static Scintigraphy: Tc99 is used to check for renal function. This susbtance is taken up by tubular cells according to their function. This is done to identify ectopic kidneys and pseudo-tumours. N.B. Dynamic and Static Scintigraphy are also called Isotope Scans. They are used for investigating kidney damage caused by urinary tract infection in children.

URINARY TRACT INFECTION (UTI): 1. 2. 3. 4. 5. 6.

Bacteriuria: presence of bacteria in the urine. It can be symptomatic and asymptomatic. Urethritis: infection of the urethra Cystitis: bladder infection Pylonephritis: infection in the kidney Prostatitis: infection in the prostate Epididymo-orchitis: infection of the testes and epididymis

RISK FACTORS

1. 2. 3. 4. 5. 6. 7.

Female Sexual intercourse Pregnancy Menopause Immunosuppression Diabetes Mellitus Urinary obstruction due to stones or tumour, faecal impaction, malformation and catherization.

A recurrent urinary tract infection is a furthur infection with a new organism. Common in females. Usually 2 or more infection in a year with different organisms. A relapse is a further infection with the same organism. Usually 2 or more infection within a year. Uncomplicated UTI: is when you develop urinary tract infection with normal renal function and normal GU tract anatomy. Complicated UTI: This is UTI in the presence of abnormal GU tract or abnormal renal function e.g. urinary obstruction. N.B: Assume all UTI's in men and children (whether boy or girl) without any risk factors as complicated. UTI in a catheterised patient: The urine may turn purple in the catheter bag due to breakdown of urine substances into pigments by bacterial enzymes Common causes of UTI are as follows and in this order:

1. 2. 3. 4.

E.Coli Proteus Klebsiella Pseudomonas.

Symptoms:

• • • •

Cystitis: frequency, dysuria, urgency, haematuria, suprapubic pain Acute Pyelonephritis: high fever, vomiting, loin pain Prostatitis: flu-like symptoms, lower backache, swollen or tender prostate on per rectal examination. Epididymo-orchitis: swollen, painful testes.

Investigation:

1. 2. 3. 4.

Urine dipstix will show nitrates, white cells or there is presence of blood Mid stream urine for microscopy, culture and sensitivity Cystoscopy if bladder cancer is suspected eg. in an elder patient with recurrent UTI Ultrasound scan for UTI in children, men and if recurrent in women in order to look for predisposing factors.

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• • • • •

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In young men and women, the most likely cause is renal stones so investigate with IVU If IVU is normal perform an ultrasound scan and vice versa In children preform an ultrasound scan first Suspect bladder cancer in elderly patients with recurrent UTI so perform Cystoscopy In children, UTI can cause kidney damage and lead to kidney fibrosis which may cause hypertension whey they grow up so perform an isotope scan to check for any damage.

Treatment:

1. Bacterial UTI in women: Trimethoprim, nitrofurantoin or cefalexin. 2nd line is co-amoxiclav. 2. Acute Pyelonephritis: Co-amoxiclav 3. Bacterial UTI in men: Levofloxacin NB. In pregnant women with UTI, use amoxicillin and cefalexin

DIFFERENTIATING SEXUALLY TRANSMITTED INFECTIONS FROM UTI 1. Gonorrhea: purulent discharge, symptoms usually appear 2-3 days after unprotected sexual intercourse. Short incubation period of gonorrhea (3.5g/24hr, Hypoalbuminaemia 80% are due to Glomerulonephritis, DM, Amyloidosis, SLE and Drugs. Complications:

1. Increased risk of infections due to loss of immunoglobulins. 2. Thromboembolism e.g. deep vein thrombosis/pulmonary embolism, renal vein thrombosis - due to increased clotting factors.

3. Hyperlipidaemia- increase cholesterol and triglycerides production by the liver in response to low oncotic pressure. Investigation: Renal Biopsy to find out what type of glomerulonephritis it is. Treatment:

1. Reduce oedema with loop diuretic e.g. Furosemide 2. Reduce proteinuria ACE inhibitor or Angiotension receptor blocker (ARB) should be started. 3. Treat the underlying cause

GLOMERULONEPHRITIS:

(inflammation of the glomeruli)

Is a common cause of End Stage Renal Failure Presentation: pastedGraphic.png

Investigation: 1. ANA

2. 3. 4. 5. 6. 7.

ANCA ASOT Anti-ds DNA Anti-aBM Urine for protinuria and heamaturia Renal Biopsy

TYPES OF GLOMERULONEPHRITIS 1.Thin basement membrane nephropathy: It is an autosomal dominant disease. It is benign persistant microscopic heamaturis in children. Reassure.

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2.Minimal change disease: common cause of nephrotic in children. On light microscopy looks normal but on electron microscope shows Fusion of Podocytes. Treatment: Cyclophosphamide 3.Membranous Nephropathy: presentation usually is Nephrotic Syndrome. It is associated with SLE, Malignancy, Gold, Penicillin, Rheumatoid Arthritis. Renal Biopsy- shows thickened basement membrane, Rx: Steroids + Cyclophosphmide 4.Ig A Nephropathy (Berger's Disease): typically presents as Macro or Micro-Heamaturia and is typically in a young male child with hematuria 1-2 days after URTI, Treatment: Cyclophosphamide 5.Focal Segmental Glomerulosclerosis: associated with HIV, Hepatitis, Ig A Nephropathy and it can be Idiopathic. Renal Biopsy shows some glomeruli have scarring of certain segments. Treatment: Steroids, cyclophosphamide, cyclosporin. 6.Proliferative Glomerulonephritis: the chief cause is Post- Strep glomerulonephritis. Typically 1-12 weeks after sore throat (URTI). Presentation is Nephritic Syndrome which consists of Hematuria, Proteinuria and Hypertension. It is the same as acute glomerulonephritis. Treatment: Supportive 7.Rapidly Progressive Glomerulonephritis: There are many causes, especially anti-glomerular basement membrane (Goodpasture's, SLE, IgA) Renal biopsy shows Cresent (macrophage) in bowman's Capsule. Treatment: high dose steroids and Cylophosphamide. 8.Mesangiocapillary Glomerulonephritis- Biopsy shows proliferation of the mesengial cells and presents as Nephrotic Syndrome, Rx- Steroids 9.Henoch-Schonlein Purpura- is a systemic variant of IgA nephropathy causing small vessel vasculitis. Smptoms are Purpuric rash on extensor surface typically on legs, abdominal colic, polyarthritis and GN.

ACUTE KIDNEY INJURY The term acute renal failure has now changed due to acute kidney injury. It is defined as deterioration in renal function occurring over hours or days. Biochemically is detected by raising Urea and Creatinine. Causes: Commonest causes are ischaemia, sepsis and nephrotoxins. The causes can be classified as: 1. Pre-Renal: Renal hypoperfusion due to hypovolaemia (vomiting, dehydration, diarrhea or bleeding), sepsis (causing systemic vasodilatation), liver failure, renal artery stenosis. 2. Intrinsic renal: ATN damage to tubular cells due to ischaemia or nephrotoxins such as haemoglobin, drugs (antibiotics, NSAIDS or ACEI), Myoglobin. 3. Post-Renal: Caused by urinary tract obstruction. Common causes of obstruction are benign prostatic hypertrophy, stones or stricture.

MANAGEMENT: Treat the underlying cause Prerenal: Correct volume depletion, treat sepsis if present Intrinsic Renal: Refer early to nephrology. Post-renal: Catheterise and consider CT of renal tract. Refer to urology if obstruction is likely. When deciding treatment of renal injury find out if it is chronic or acute as the treatment is different. Is the injury acute or chronic? Suspect chronic injury if the following are present:

• • • •

The kidneys are small (10 • Desmopressin to increase Factor VIII activity

INDICATION OF DIALYSIS IN ACUTE RENAL FAILURE: 1. 2. 3. 4. 5. 6.

Refractory Pulmonary Oedema (not responding to IV furosemide) Persistant Hyperkalemia >7mmol/l (not responding to insulin or salbutamol) Severe Metabolic Acidosis pH 200) Hyperlipidemia – Statins Pulmonary oedema - Furosemide Anemia – Erythropoeitin Acidosis - consider sodium bicarbonate

Urea and creatinine will be increasing as number of glomeruli decreases so treat hyperkalemia. If hyperkalemia in chronic renal failure then treat with insulin and glucose. Long term treatment of chronic renal failure is different from treatment of acute renal failure. In chronic renal failure urea and creatinine will be increasing and it is not a major concern as we know it will be increasing. 1. Long term dialysis (in end stage renal failure) 2. Kidney transplant.

URINARY TRACT STONES Causes:

1. Hyperparathyroidism: Increased parathyroid hormone leading to increased serum calcium levels leading to formation of 2. 3. 4. 5. 6. 7. 8. 9. 10.

bilateral renal stones or recurrent renal stones. Investigation: serum calcium and parathyroid hormone Idiopathic Hypercalcaemia Sarcoidosis there is increased serum calcium and increased ACE Increased vitamin D leads to hypercalcaemia Gout: Increased uric acid forms urate stones which are radiolucent on KUB. Urate stones are common conditions like gout, myeloma and tumour lysis syndrome Familial metabolic causes e.g cystinuria, hyperoxaluria, hyperuricuria Infection predisposes to stones and stones predisposes to infection. Obstruction of urinary tract e.g. stricture on ureter Diet: tea, spinach, and rhubarb predisposes to oxalate stones if all biochemical and imaging in normal check dietary history. Dehydration in long distance runners and also in people who work in hot climate.

TYPE OF RENAL STONES

1. Calcium stones usually combined with phosphates or oxalate.

1. Triple phosphates stones (struvite) consists of magnesium, ammonium and calcium. They are also called Staghorn.

1. Urate stones normally associated with gout and myeloma or after Tumour Lysis Syndrome. Tumour Lysis Syndrome: Radiotherapy/chemotherapy to break down the cancer cells, causes increased urate, forming stones. Gout Symptoms: red, swollen, painful joints especially the big toe. Myeloma usually present with back pain, increased ESR, proteinuria and anaemia. Renal stone symptoms:

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1. Renal stones: renal colic which is pain in the loin, +/- Heamturia. 2. Ureteric stones: ureteric colic which is right /left iliac fossa pain radiates to the groin +/- haematuria 3. Bladder stones: pain in the suprapubic area plus haematuria.

INVESTIGATIONS IN RENAL STONES: 1. Initial is KUB X-ray (can visualise 99% of stones, except urate stones which are radio-lucent) 2. IVU is the investigation of choice in all renal stones whether it is in the ureter or kidney. 2. Mid-stream urine if there is fever because that means there is infection caused by pre-existing stone. 3. If recurrent stones or bilateral stone's and pancreatitis think of hyperparathyroidism Investigation is serum calcium and then parathyroid hormone. 4.If symptoms of obstruction then ultrasound scan to check for hydronephrosis.

URINARY RETENTION: (common in men) 1. BENIGN PROSTATE HYPERPLASIA: is the commonest cause (due to poor stream of urine) Symptoms: frequency, nocturia and dribbling. But there is haematuria in BPH. 2. CLOT RETENTION: Usually elderly or middle aged male. The patient is usually with bladder cancer. The tumour bleeds and clots block the urethra. Remember, painless haematuria in an elderly patient is always bladder cancer until proven otherwise. 3.SPINAL CORD COMPRESSION: There is usually sudden onset of urinary retention and bowel symptoms like constipation, incontinence and lower limb weakness or sensory loss. 4.FAECAL IMPACTION: Typically in elderly patient or young child with history of constipation. On examination there can be palpable mass in the abdomen usually left iliac fossa. Faecal impaction presses on the Urinary Tract --> Urinary Retention --> UTI --> Confusion in elderly. There may be overflow diarrhea. Treatment: Quick evacuation of the faecal impaction with a phosphate enema per rectal if it is causing UTI. 5. MULTIPLE SCLEROSIS: Typically in a patient with already diagnosed multiple sclerosis. Treatment: Intermittent self catheterisation. 6. In children Meningocele: is the herniation of meninges like dura and arachnoid or meningomylocele and there is cord involvement. Treatment: If the child is developing well and is old enough then intermittent self catheterization.

URINARY INCONTINENCE: 1. Urge incontinence: the cause is detrusor overactivity or instability. It is found both in nulliparous and multiparous women. Detrusor is the muscle of the bladder and it's overactivity causes a sudden desire to pass urine. 2. Stress incontinence: small quantities of urine escape as intra-abdominal pressure rises e.g. during sneezing or cough in the absence of bladder contraction. 3. Mixed incontinence: when there is incontinence of urine whether a patient laughs, sneezes or not. 4. Overflow incontinence: this happens when there is incomplete bladder emptying, there is dribbling of urine e.g. benign prostatic hypertrophy. 5. Fistula: Usually form after surgery eg. hysterectomy, or if there is an inflammatory condition eg. Crohn’s disease, diverticulitis. Patients complain of constant leakage of urine. There may also be air or faecal matter in the urine. N.B: In children incontinence is normal, all you need to use is incontinent pants

STRESS INCONTINENCE: Continence in women is maintained by the proximal and distal sphincter which maintains the pressure in the urethra to be higher than that of the bladder. There are also other structures like pelvic muscles which supports the urethra and helps to maintain this higher pressure. This pressure is also higher than that of the intra-abdominal. Factors that may contribute to incontinence:

1. 2. 3. 4. 5.

Pregnancy: raises intra-abdominal pressure Delivery: causes weakness of the pelvic muscles therefore lowers the pressure in the urethra. Menopause: lack of oestrogen also weakens the closure of the sphincter, causing decreased pressure in the urethra. Obesity: increases intra-abdominal pressure, therefore losing weight might help Uterine prolapse

Cysotocele: upper front wall of the vagina and bladder attached to it bulges into the vagina. Urethrocele: lower anterior of the vagina wall bulges, this will displace sphincter and impaired sphincter mechanism causes decreased urethra pressure which leads to stress incontinence. Enterocele: small intestine bulges into the posterior wall of the vagina may contain intestine in the pouch of douglas. Uterine prolapse: there is a dragging sensation or feeling of something coming down which gets worse by day. Cystitis, frequency, stress incontinence and difficulty in defecation along with feeling of pressure in the perineum.

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Rectocele: part of the rectum bulges into the posterior wall of the vagina. Treatment of uterine prolapse:

1. Ring pessaries for temporary treatment or for very frail women who cannot undergo surgery. 2. Surgery

INVESTIGATIONS IN URINARY INCONTINENCE:

1. Mid-Stream Urine: if infection (dysuria, frequency, fever) 2. Filling urodynamic assessment 3. Voiding urodynamic assessment - The bladder is filled with normal saline and at the same time pressure in the bladder and intra-abdominal pressure is measured. Bladder pressure will always be high during incontinence. The abdominal pressure during incontinence will differentiate between stress incontinence and urge incontinence.

• If the abdominal pressure is also high, then the diagnosis is stress incontinence. • If the abdominal pressure is normal, then the diagnosis is urge incontinence or detrusor instability. Voiding Urodynamic - is assessed during voiding. If the bladder is filled with 500ml saline and the patient urinated only 350ml it is regarded as abnormal. If the voiding speed is less than 15 ml/sec it is considered abnormal. Treatment of stress incontinence:

1. 2. 3. 4. 5.

Pelvic floor exercises Oestrogen if post menopausal Physiotherapy e.g.vaginal cones Drugs e.g. duloxetine Surgery for severe stress symptoms e.g. colposuspension or bladder neck surgery.

Treatment of detrusor instability:

1. 2. 3. 4. 5.

Pelvic exercise Avoid caffeine Bladder training to increase time between voiding Pelvic floor physiotherapy Oxybutin

Fistula Causes:

• Inflammatory conditions - usually diverticulitis and crohn’s disease (inflammatory bowel disease) • Malignancy - usually rectal carcinoma • Iatrogenic - post surgery and radiotherapy Types of fistulas:

• Enterovesical - e.g. colovesical usually presents with pneumaturia (gas in the urine) and faecaluria (fecal matter in the urine)

• Enterovaginal - eg colovaginal. Passage of stool or flatus via the vagina is pathognomonic of a colovaginal fistula. It may also present with frequent vaginal infections or copious vaginal discharge.

NB. Symptoms of the chronic disease causing the fistula may be present. These symptoms will help to determine the cause of the fistula. Resource start date

2013-06-26 09:49

Resource end date

2023-06-27 09:49

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• ◦ ◦ ◦ ◦ • +44 0208 9800 039 +44 0794 0433 068 • • • • •

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Neurology PLAB 1 Notes

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Neurology

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SAMSONPLAB ACADEMY Bow Business Centre Bow Road 153-159 E3 2SE, London Telephone: +44(0)2089800039 Mobile: +447940433068 Email: [email protected]

Lecture notes: Neurology The brain is comprised of the left and right hemisphere. Each hemisphere has four lobes. Lobes 1. 2. 3. 4.

Frontal lobes Temporal lobes Parietal lobes Occipital lobes

Left hemisphere:

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• • • •

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Is usually the dominant hemisphere 70% of all left handed people have the left hemisphere as dominant Almost all right handed people have the left hemisphere as dominant The dominant hemisphere contain areas of speech

Right hemisphere: •

Usually it is non-dominant, meaning no areas of speech

There are 2 areas of speech: Broca’s Area • • • • • • •

Broca’s area is located in frontal lobe If affected, patient will have expressive aphasia (Broca’s aphasia) Difficulty to find right words Speech is slow Comprehension is intact but Coherence is lost Writing and reading are impaired Difficulty in naming objects

Wernicke’s Area • • • • • • •

Reading + writing relatively maintained Wernicke’s area is located in the temporal and parietal region If affected, it causes Receptive Aphasia / Dysphasia Fast, fluent speech, full of empty words Comprehension is lost but coherence is maintained Difficulty in understanding Comprehension is lost, coherence is maintained

Dysphasia: It is a disorder of speech. There are two types: 1. 2.

Nominal aphasia: difficulty in naming objects (Broca’s aphasia) Global aphasia: Broca’s aphasia and Wernicke’s aphasia where patient cannot understand and express himself.

Agraphia is: Disorder of writing Alexia is: Disorder of reading Dysarthria: (slurred speech) Disorder of articulation e.g. in alcoholics or cerebellar problems due to loss of coordination of the muscles of the tongue Dysphonia: Disorder of speech volume e.g. vocal cord lesion(e.g. laryngitis), recurrent laryngeal nerve palsy Dyspraxia: Inability to do complex movements. There are different types: 1. 2. 3.

Gait dyspraxia Dressing dyspraxia Constitutional dyspraxia (building)

Ataxia is: Unsteadiness or lack of balance

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Brain lesion Effects of Lesion on the brain: A lesion can do 2 things to the brain Causes destruction/compression on the brain: there will be focal neurological signs like weakness of the legs, visual symptoms, dysphasia sensory loss 2. Can cause irritation of the brain and cause functional problems like epilepsy or hallucinations and delusions. 1.

Focal Neurological Signs: 1. Frontal lobe: • • • • •

Personality change Intellectual impairment Broca’s aphasia (if dominant hemisphere) Mono or hemiparesis Urinary Incontinence

2. Temporal lobe: • • • • • •

Memory loss (amnesia) Déjà vu (a feeling everything is familiar) Je’mais vu (failure to recognise situations which have been encountered before) Wernicke’s aphasia if dominant hemisphere Upper quadrant anopia Agnosia (loss of perception)

3. Parietal lobe: • • • • •

Sensory loss Astereognosis (failure to recognise objects by touch) Loss of 2 point discrimination Wernicke’s aphasia (if dominant hemisphere) Lower quadrant anopia

4. Occipital lobe: • •

Homonymous hemianopia Cortical blindness due to bilateral occipital lobe infarction (patient is blind but does not understand that he is blind. He has no insight to his blindness)

5. Cerebellum (is mainly responsible for coordination): ◦ ◦ ◦ ◦ ◦ ◦ ◦ ◦ ◦

Diplopia Dizziness Nystagmus Dysarthria (slurred speech) Hypotonia Past pointing Dysdiadokinesis Heel-shin test positive Ataxia (cerebellar ataxia)

6. Cerebellopontine angle • •

There will be cerebellar signs Cranial nerves V, VII and VIII are affected together, because they pass through the cerebellopontine angle e.g. acoustic neuroma ((schwanoma) tumour of the VIII nerve)

CORTICO-SPINAL TRACT (Pyramidal system - motor system): Nerve fibres start in the cortex of the brain and end in the anterior horn cells of the spinal cord. The anterior horn cells are a group of nuclei. Each part of the brain cortex is responsible for one part of body

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1. 2. 3. 4. 5. 6. 7.

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Cortical Ischaemia - Contralateral monoparesis Cortical Ischaemia - Contralateral hemiparesis Brain stem - Contralateral hemiparsis (cranial nerves will be affected aswell) Cervical spine lesion - Ipsilateral hemiparesis Cervical spine lesion - Tetraplegia or quadriplegia Ipsilateral monoparesis – Left leg for example Complete section of the spinal cord – paraplegia

Upper Motor Neuron signs (UMN):

1. 2. 3.

(lesion is above anterior horn cell)

Hyperreflexia Hypertonia Upgoing /extensor plantar reflexes (Babinski Sign)

Lower Motor Neuron signs (LMN): (lesion

is on the anterior horn cell)

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1. 2. 3. 4. 5.

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Hypotonia Hyporeflexia Flexor plantar Muscle wasting Muscle fasciculations

Motor Neurone Disease (MND): This is damage to anterior horn cells and nuclei. Only the motor system is affected. Symptoms: 1. 2.

Weakness in the limbs Cranial nerve damage causing dysphagia and speech problems.

Common in middle aged men aged between 35-55 years.

Bulbar Palsy: (Cranial Nerves IX-XII) LMN lesions of muscles of mastication, swallowing and talking Signs: 1. 2. 3. 4. 5.

Muscle fasciculations Tongue fasciculations Jaw jerk normal or absent Speech is quiet Donald duck speech (nasal speech)

Pseudobulbar palsy: Lesion is above the mid-pons. UMN lesion of muscles of tongue, chewing, swallowing and facial muscles.

Signs: 1. 2. 3.

Increased jaw jerk Unprovoked sorrow Mood incongruence

N.B: In MND there is: • • •

NO sensory loss only Motor loss NO sphincter disturbances Eye muscles are NOT affected, which differentiates it from myasthenia gravis.

SENSORY SYSTEM:

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N.B: The posterior column carries the light touch, position and vibration. It enters the spinal cord and remains on the same side until the fibres reach the medulla oblongata where they cross to the opposite side.

Spinothalamic tract carries the pain and temperature fibres. It crosses the spinal cord within the first 2 segments. 1. Lesion in the brainstem will cause sensory loss on the same side of the face and contralateral sensory loss in rest of the body below the face. 2. If the lesion in the thalamus, sensory loss occurs on the same side of the face as on the rest of the body. 3. Brown Sequard syndrome: Hemi-section of the spinal cord will cause sensory loss on the same side due to damage in posterior column and loss of pain and temperature on the contralateral side due to damage of spinothalamic tract. Causes include trauma, tumours etc. 4. Cord lesion will cause loss of pain and temperature only and usually in a segmental pattern. Common cause of cord lesion is syringomyelia.

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II CRANIAL NERVE: Optic nerve

NB: The optic nerve consists of medial and lateral fibres. The media fibres cross and the lateral fibres remain on their side. 1. 2.

3.

4.

5. 6. 7.

8.

Lesion on the retina: causes include retinal detachment or haemorrhage. A lesion will cause scotoma. A scotoma is a small area in the patient’s vision where he/she cannot see. Lesion on the optic nerve: common cause is multiple sclerosis, which causes optic neuritis. Symptoms include sudden loss of vision in one eye and there is usually dull pain when moving the eye. It will cause monocular blindness. Lesion on the optic chiasma: common cause is pituitary tumour, which compresses the optic chiasma. Other causes include craniopharyngioma and meningioma. Visual field defect is bitemporal hemianopia. Lesion on the optic tract: common causes include stroke and tumour. Visual field defect is noncongruous homonymous hemianopia. The visual field defect is always on the opposite side to where the lesion is. Lesion in the temporal lobe: causes include stroke and tumour. Visual defect is homonymous upper quadrantanopia. The visual field defect is always on the opposite side to where the lesion is. Lesion in the parietal lobe: causes include stroke and tumour. Visual field defect is homonymous lower quadrantanopia. Lesion on the occipital lobe: causes include stroke and tumour. Visual field defect is congruous homonymous hemianopia. Can be with macula sparing or non-macula sparing. If it is macula sparing then the cause is posterior cerebral artery. The visual field defect is always on the opposite side to where the lesion is. Bilateral lobe lesion e.g. bilateral stroke causing cortical blindness.

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BLOOD SUPPLY OF THE BRAIN:

ACA = Anterior cerebral artery MCA = Middle cerebral artery PCA = Posterior Cerebral Artery

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A. Vertebro-basilar artery supplies: 1. 2. 3.

Posterior Cerebral Artery which supplies the occipital lobe Cerebellum Brainstem

(Vertebro-basilar insufficiency/atherosclerosis) B. Internal Carotid artery supplies: 1. 2.

Anterior Cerebral Artery which supplies the frontal lobe and inner aspect of the hemisphere Middle Cerebral Artery which supplies the outer aspect of the hemisphere

(Carotid artery disease) C. External Carotid:

supplies the eye. It causes amaurosis fugax.

Areas of the brain supplied by the cerebral arteries.

Vertebro-basilar Atherosclerosis: Causes hypoperfusion of the cerebellum leading to the following symptoms: 1. 2. 3.

Dysarthria Diplopia Nystagmus

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4. 5. 6. 7. 8.

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Hypotonia Ataxia Finger nose past-pointing Dysdiadokinesia Vertigo

Atherosclerosis of the posterior-inferior cerebellar artery or vertebral artery causes lateral medullary syndrome which is ischaemia to the brain stem and cerebellum leading to Horner’s syndrome and cerebellar signs.

Horner’s Syndrome: 1. 2. 3. 4.

Ptosis (incomplete) Miosis Enopthalmus Anhydrosis (loss of sweating on the ipsilateral side of the face) This is due to damage to sympathetic fibbers

Subclavian Steal Syndrome Subclavian artery stenosis proximal to the vertebral artery, causing blood to be ‘stolen’ down the axillary artery down the arm, leading to brain ischaemia. Suspected if you have a different blood pressure in each arm, usually >20mmHg. N.B: Thoracic aortic aneurysm will cause different blood pressure in each arm aswell.

DEMENTIA: Main feature is memory loss. Impaired cognition with intact consciousness causes: 1.

• • • • • • • • •

Alzheimer’s Disease: Commonest cause of dementia in the UK Gradual onset Visuo-spatial dysfunction e.g. getting lost when taking a walk in the park or when driving. Progressive memory loss and cognition Normally in old age Pathologically: Neurofibrillary tangles and senile plaques Patient may be previously fit and well There are behaviour changes: aggressive, emotionally liable, depression May have seizures in the late phase.

Investigations: Rule out the following reversible causes (dementia screen) a. b. c. d. e.

B12/Folate deficiency TSH (hypothyroidism) HIV test Thiamine deficiency Syphilis serology

CT scan: to rule out vascular dementia, subdural haematoma or brain tumour. Diagnosis is made by mini-mental state examination or mental state examination Treatment: Donepazil 2. Vascular Dementia/ Mult-infarct Dementia: • • • • • • •

Second commonest cause of dementia in the UK Sudden onset Due to multiple TIA’s or Stroke History of hypertension or diabetes mellitus History of ischemic heart disease History of atherosclerosis (intermittent claudication) There is STEPWISE DETERIORATION in cognition and memory

Investigation: CT scan brain (which will show brain infarction)

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3. Fronto-temporal lobe Dementia: • • •

Early personality change Visual spatial functions are relatively preserved from the beginning Early intellectual impairment

4. Lewy Body Dementia: • • •

Hallmark of Lewy Body dementia is FLUCTUATING loss of memory It is associated with Parkinsonism (bradykinesia, tremors, rigidity) Pathological finding = Lewy Bodies

5. Huntington’s Disease: • • • •

There is a strong family history It is autosomal dominant (1:2 inheritance) Usually in a young or middle aged patient Chorea

6. Pseudo-dementia: • • •

Due to depression Symptoms of depression like low mood, poor sleep, loss of appetite, loss of interest in daily activities Responds to antidepressants

7. Pick’s Dementia: • • • •

1.

Mainly cognition impaired Memory is usually normal (they score very well on the memory test) Unusual sexual adventures and talking about their sexual life openly It may lead to stealing Wilson’s Disease:

This is accumulation of copper in different organs due to deficiency of a protein called ceruloplasmin which transports copper in the body • Copper accumulates in different organs of the body: •

a. b. c. d. •

1.

Copper Copper Copper Copper

deposition deposition deposition deposition

in in in in

the the the the

brain leads to dementia liver leads to liver disease joints leads to joint pain eye will cause Kaiser Fischer rings

Investigation: Serum copper Wernicke’s Korsakov Syndrome:

This is brain damage due to deficiency of Vitamin B1, also called thiamine It is common in alcoholics The patient always has liver disease Consists of Wernicke’s encephalopathy: which is a triad of confusion, ataxia and opthalmoplegia. Patient will also have flapping tremor and headache. • Korsakov’s Psychosis: confabulation due to short-term memory loss. Confabulation is making up stories due to short-term memory loss. • Treatment: Thiamine • • • •

11. Creutzfeldt-Jacob Disease (Prion Disease/Mad Cow Disease): • • • • •

1.

•

Prion is an altered protein which can be transmitted through blood transfusion or surgical instruments from one patient to another It can transform other proteins to become abnormal therefore it is infective Common in haemophilics with history of previous blood transfusion Accumulation of these prions in the brain causes dementia No treatment available HIV dementia: Must be an HIV patient

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• • •

1.

• • •

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History of blood transfusion or IVDU or homosexuals HIV patients are usually immune-compromised and usually also they have tuberculosis Dementia present with confusion but this is progressive confusion for weeks and months Age-related forgetfulness: Patient has insight to problem It is normal forgetfulness which everyone develops with age The patient is usually concerned and not happy about it

N.B: Patients with true dementia have no insight in to the problem.

Cranial Nerves i. Olfactory:

if it is affected patient will have anosmia (loss of sense of smell)

i. Optic nerve:

please see above

Damage to this nerve will cause diplopia in different directions. There is also dilated pupil and complete ptosis. Diplopia on looking up means third nerve palsy but it can cause diplopia in other directions as well as it innervates 4 muscles of the eye:

i. Oculomotor:

1. 2. 3. 4.

Superior Rectus Inferior Rectus Medial rectus Inferior oblique The eye deviates downwards and outwards.

i. Trochlear:

Diplopia on looking down i.e. walking down the stairs or reading. But dilated pupils will mean 3rd nerve palsy and 4th nerve palsy does not cause dilated pupils. The 4th nerve innervates the superior oblique (SO4), which pulls the eye down and medially. Sensory loss on face of ophthalmic, maxillary or mandibular division i.e. loss of sensation on the face. It innervates the involuntary muscles and muscles of mastication (masseter muscles and temporalis). It also innervates the cornea, so can cause corneal anaesthesia or loss of the corneal reflex and jaw jerk reflex.

i. Trigeminal nerve:

i.

Trigeminal Neuralgia is electric, stabbing, knife like, shooting painon the face. Treatment: carbamazepine.

i. Abducent nerve:

It innervates the lateral rectus muscles (LR6) and if it is affected there will be diplopia on looking sideways. Dilated pupils would indicate 3rd nerve palsy. Failure to close the eye, loss of nasio-labial folding, deviation/dropping of angle of mouth, loss of taste in anterior 2/3rd of the tongue.

i. Facial nerve: i. ii.

Lower motor lesion- Both face and forehead are affected Upper motor lesion- Forehead is spared (not affected)

N.B: It innervates the voluntary muscles of the face (muscles of expression) i. Vestibulocochlear nerve:

Damage will cause deafness and balance problems (sensory ataxia – dizziness and vertigo). It has connection with the posterior column.

i. Glossopharyngeal:

i. Vagus:

Innervates Tongue and Pharynx rd i. Loss of taste on Post 1/3 of tongue ii. Deviation of palate to one side

Loss of gag reflex plus it innervates a lot of visceral organs including the heart.

i. Accessory nerve:

There will be failure to shrug shoulders on resistance because it innervates trapezius and also failure to turn head sideways on resistance because it innervates sternocleidomastoid muscle (SCM).

i. Hypoglossal nerve:

Deviation of tongue one side. The lesion is on the same side where tongue

deviates

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MENINGITIS: Inflammation of the meninges of the brain Causes:

a.

Bacterial

1. 2. 3. 4.

Streptococcal pneumonia is the commonest in adult Neisseria meningitides usually if there is rash Tuberculosis in patients from endemic areas like Africa and Asia Listeria monocytogenes should be considered if more than 50 years of age

a. b. c. d.

Viral Protozoa Leukaemic Infiltration if there is history of leukaemia Malaria in patients with recent history of travel to endemic areas like Africa

Symptoms:

1. 2. 3. 4. 5.

Headache Fever Photophobia Vomiting Rash - suggests meningococcemia and the cause is Neisseria meningitides

Signs: 1. 2. 3. 4.

Brudzinki’s Signs Kernig’s Sign Neck Stiffness photobia

Management of Meningitis

1.

If you suspect meningitis and you are outside the hospital (commonly in the GP) you should give 2.4 g intravenous benzylpenicillin and the patient should then be sent to hospital

1.

In hospital give intravenous third generation cephalosporin antibiotics (ceftriaxone or cefotaxime)

1.

Now look for rash. If patient has got rash then do blood culture as the diagnosis is meningococcal septicaemia. The causative organism is Neisseria meningitides.

1.

If no rash then we need to do a lumbar puncture, but check that there are no signs of raised intracranial pressure (drowsiness, papilloedema, focal neurological signs); Headache and vomiting are not very reliable signs of raised ICP in meningitis as most of the time meningitis presents with vomiting and headache.

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1.

If there are signs of raised intracranial pressure then do CT scan of the head in order to rule out raised ICP. If CT proves there is raised ICP do not do lumbar puncture as there is risk of herniation of the brain.

1.

If there are no signs of raised ICP then do lumbar puncture straight away.

If patient more than 50 years of age add cotrimoxazole to cover listeria, but if listeria has been identified then give ampicillin/amoxicillin and gentamicin.

Key Points of Management:

1. 2. 3. 4. 5. 6.

GPs should give benzylpenicillin or a 3rd generation cephalosporin (cefotaxime and ceftriaxone) before urgent transfer to hospital. Give chloramphenicol if there is a history of anaphylaxis to penicillin or cephalosporins. rd Meningococci: Benzylpenicillin or 3 generation cephalosporin for at least 5 days. rd Pneumococci: 3 generation cephalosporin or benzylpenicillin for 10-14 days. If resistant, add vancomycin. rd Haemophilus Influenza: 3 generation cephalosporin for 10 days. Listeria: Amoxicillin and gentamycin

Signs of raised ICP in general

1. 2. 3. 4.

Papilloedema Drowsiness Headache Vomiting

Lumbar Puncture

Cells

VIRAL Lymphocytes

T.B. Lymphocytes

Glucose Proteins

←→ or Slightly↓ ↑

↓ ↑

Bacterial Neutrophils and Polymorphs ↓ ↑

Normal CSF: • •

Glucose is 2.5 - 4.5 mmol/L (1/2 – 2/3 of blood glucose) Protein 0.2 - 0.5g/L (200-500mg/dl)

Prophylaxis of Meningitis Rifampicin BD (twice daily) for 2 days for all contacts including doctor and nurse e.g. nursery, classrooms. NB: prophylactic antibiotics are given only to people who have come in contact with a patient or those who are more likely to have been in contact. Complications of meningitis: 1. 2. 3. 4. 5. 6.

Deafness (especially in children – 10% of child cases) - arrange hearing test after treatment of meningitis in children. Failure to thrive in children. SIADH - causes low sodium. Treat with fluid restriction. Raised ICP - treat with mannitol and monitoring. Seizures - treat with lorazepam and then phenytoin or treat as status epilepticus. The majority of patients do not develop complications.

CNS infection in HIV: Toxoplasmosis Gondii Presents with mass like effect i.e. progressive headache and focal neurological signs

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Investigation is CT scan which shows ring enhancing lesion If signs of raised intracranial pressure give dexamethasone

Treatment is pyrimethamine and sulphadiazine Crytococcus Meningitis Presents with altered consciousness or confusion with meningism and headache Investigation is Lumbar Puncture for CSF

Treatment is amphotericin in acute state and fluconazole for maintenance

Parkinson’s Disease The hallmark of Parkinson’s disease is presence of lewy bodies and neural cell death in the pars campus in the substantial nigra. Parkinson disease does not develop until the level of dopamine falls below 20% of normal amount. Symptoms: 1. 2. 3. 4. 5.

Mask like face Shuffling gait Bradykinesia: slowness of initiation of movement Rigidity Tremor (unilateral)

Symptoms are usually unilateral and there is good response to levodopa. Symptoms are progressive Investigation:

no diagnostic test. Diagnosis is made by clinical symptoms.

Treatment: 1. 2. 3. 4. 5. 6. 7.

Levodopa Dopamine agonist cabergoline, ropirinole, Apomorphine Amantidine MAOI like selegiline Entacapone a COMT drug anticholinergic agent like benzhexol

Differential Diagnosis: Lewy Body Dementia – does not respond very well to levodopa. Parkinson’s disease does respond well to levodopa. 2. Drug induced Parkinsonism – Typical antipsychotics (haloperidol) 1.

EPILEPSY (Abnormal electrical discharge in the brain) CLASSIFICATION: 1. 2.

Partial Primary Generalised

PARTIAL: this is when electrical discharge from 1 hemisphere

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a. b.

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Focal (remains in 1 hemisphere) Secondary Generalised (spreads to both hemispheres) e.g. Jacksonian attack (jerking starts from the thumb -> hands -> body.

PRIMARY GENERALISED: Electrical discharge from both hemispheres a. b. c. d. e.

Infantile spasms (salaam attack) common in infants. This child jerks back and forth like the way muslims pray. It can also cause severe developmental delay Absent seizures -> in children. A period the child stops for about 10 seconds and then resumes what he is doing Tonic clonic Atonic (floppy) Myoclonic (twitching of the muscles of the face and the whole body)

Epilepsy: 1. 2.

Simple (no loss of consciousness) Complex (loss of consciousness)

Symptoms: 1. 2. 3. 4. 5.

Jerking (fit) Urinary or faecal incontinence Tongue biting Loss of consciousness Post-ictal status

Investigations:

1. EEG: Investigation of choice is EEG 2. CT Scan (to rule out brain tumour) a. b. c.

If seizure of new onset at night (during sleep) If seizure is associated with prolong headaches New onset focal seizures in adults (epilepsy is usually develops in a child)

Treatment: 1. 2. 3. 4.

Primary Generalised epilepsy - Sodium valproate Absence seizure - Ethosuximide Partial seizure - Carbamazapine Infantile Spasm - Vigabatrin

If seizures without any cause -> send to 1st fit clinic and advise the patient not to drive and inform DVLA. General advice to give patient: 1. 2. 3. 4.

Do not drive and advice patient to inform DVLA Avoid unsafe activities e.g. swimming alone, mountain climbing, riding a bicycle Take showers rather than bath Avoid precipitants like night club, watching TV with strobe lights on

Status Epilepticus: This is seizure lasting more than 30 minutes or repeated attacks of seizures without gaining consciousness in between.

Treatment of Status Epilepticus: IV lorazepam ↓ IV lorazepam (repeat) ↓ Phenytoin IV ↓

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Phenobarbiturate IV ↓ Anaesthetise and Intubate If after PR Diazepam if patient is still fitting and you have gained an intravenous line give IV Lorazepam Drug Side Effects 1.

Carbamezapine: Rash (in short term), Renal failure, diplopia, hyponatraemia, SIADH, neutropenia

1.

Sodium Valproate: weight gain, liver failure, tremor, sedation, rash, low platelets, hair loss

1.

Phenytoin: gum hypertrophy, cerebellar signs and depression. ↓ i. ii. iii. iv. v.

Nystagmus Diplopia Ataxia Dysarthria Dizziness

1.

Ethosuximide: bone marrow suppression, headache, lethargy, ataxia, agranulocytosis, GIT irritation.

1.

Benzodiazepines: IM injection may cause cold abscess

INTRACRANIAL BLEED: 1. Subarachnoid Haemorrhage:

• • • •

Common in young patients 30-50 years Cause is Berry aneurysm - located at posterior or anterior communication artery. May present with collapse while exercising It is associated with Polycystic Kidney Disease, coarctation of aorta, Ehler-Danlos syndrome.

Signs and symptoms 1. 2. 3. 4. 5.

Sudden onset headache at the back of the head (occipital) Projectile vomiting Neck stiffness Photophobia There is usually family history

N.B: Sudden onset of headache is always subarachnoid haemorrhage until proven otherwise. Severe headache but no history of head injury. Investigation:

1. 2.

CT scan head If CT scan head does not show bleeding, do lumbar puncture at least 12 hours after onset of headache. Usually you look for bilirubin in the CSF (xanthochromia).

Treatment: 1. 2. 3.

Nimodipine for the pain Refer to neurosurgeon Treatment is usually surgery (clipping of the aneurysm)

2. Subdural Haematoma:

• • • • • • •

Common in elderly with recurrent falls Also in alcoholics and boxers due to recurrent head injury changing level of consciousness (progressive drowsiness) Trauma may happen long time and patient may forget about it e.g. 2 weeks ago Signs of raised ICP which are headache, papilloedema and vomiting Focal neurological signs i.e. weakness of the legs or sensory loss Can present with cognitive impairment

Investigation:

CT scan

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Treatment:

1. Refer to neurosurgeon for evacuation of haematoma 2. Surgery - Burr hole (done as an emergency to relieve increased intracranial pressure) 3. Extradural Haematoma:

• • • • • • • •

Rapid deterioration of consciousness There is lucid interval i.e. in minutes to hours Almost/always there is history of head injury Signs of raised ICP (headache, vomiting and papillaoedema) Fits Focal neurological signs Up going plantar reflexes (Babinski sign) Monoparesis

Investigation:

CT scan

Treatment: 1. Surgery for evacuation of haematoma 2.Burr hole may be used in emergency to relieve the pressure 4. Intracerebral bleeding (haemorrhagic stroke) • • •

Elderly patient with history of hypertension, usually uncontrolled or untreated hypertension. Sudden loss of consciousness, preceeded by headache History of ischaemic heart disease or diabetes mellitus

• • • • •

Normally focal neurological signs Up going plantar reflex Dilated pupils UMN signs in limbs Intracerebral bleed is same as haemorrhagic stroke

Investigation:

CT scan head.

Treatment: Refer to neurosurgeon to evacuate haematoma

Differential Diagnosis for Focal Neurological Signs: Focal neurological signs are impairments of nerve or brain function that affects a specific region of the body. For example: weakness of the arm, or the leg etc. Differential diagnosis:

1. 2. 3. 4. 5. 6. 7. 8. 9. 10.

Intracranial bleeding Meningitis Multiple Sclerosis Brain or spinal tumour Syringomyelia Trauma Migraine Stroke Motor Neurone Disease Myasthenia Gravis

FOCAL NEUROLOGICAL SIGNS: 1. Multiple sclerosis: Autoimmune condition. It is due to demyelination of the nerve fibres in the central nervous system (brain and spinal cord). It only affects CNS not peripheral nervous system. Patients are usually young females, typical age 18-30 years old. There is mono-symptomatic presentation depending on the location of the lesion and lesions are scattered in neuro-anatomy. Optic neuritis, sudden loss of vision with dull pain in the eye, then symptoms will resolve and then come back b. Spinal Cord - Weakness in the limbs, urinary retention/incontinence c. Optic Disc - Papilloedema a. Optic Nerve -

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d. Brainstem - Weakness in the leg or sensory loss with e. Cerebellum - Dysarthria, nystagmus, ataxia, etc.

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cranial nerves palsy.

Symptoms appear on by one and each time the lesion is in a different location.

Classification: Remitting/Relapsing MS: symptoms comes and go (symptoms stay for weeks-months, then disappear completely). This is commonest form 2. Primary Progressive MS: from the beginning the symptoms keep progressing without remission. 3. Secondary Progressive MS: Initially it was remitting/relapsing MS then symptoms started progressing. 1.

Investigation:

a.

MRI scan of the brain or spinal cord depending on the symptoms. This is the investigation of choice

a.

Lumbar Puncture - look for monoclonal bands in CSF

Diagnosis is made by MRI and clinical signs Treatment: During attack ↓ IV Methylprednisolone

During remission ↓ Interferon α +b (disease modifying drugs)

CEREBROVASCULAR ACCIDENT:

Consists of stroke and transient ischaemic attack (TIA). The cause for both are the same. Brain ischemia: results in brain infarct Causes: 1. 2. 3. 4.

Thrombosis Emboli Thromboembolism Haemorrhage

Patients are elderly with sudden onset of symptoms.

Cardiovascular Accident 1. Stroke: symptoms >24 hours 2. TIA: symptoms intracerebral haemorrhage (associated with increased blood pressure, uncontrolled or untreated hypertension)

Symptoms: 1.

Carotid atherosclerosis or carotid artery disease: a. b. c. d. e.

Frontal lobe - hemiparesis, monoparesis, dysphasia if dominant Temporal lobe - memory loss Parietal lobe - sensory loss Eye - amarousis fugax If dominant hemisphere aphasia/dysphasia

2. Vertebrobasilar artherosclerosis or vertebrobasilar insufficiency:

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a. b. c. d. e.

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Dysarthria Vertigo Nystagmus Cerebellar ataxia Hypotonia

3. Brainstem: Cranial nerves are involved and causes difficulty swallowing ( UMN sign lesions in limbs )

A. Investigations to find the cause: • • • • • • • •

If Atrial Fibrillation then Echocardiogram to see intra-cardiac emboli If recurrent Myocardial Infarction then Echocardiogram to see mural thrombi If Carotid bruit then Doppler ultrasound of the neck If history of ischaemic heart disease, it means atherosclerosis is present then Doppler ultrasound (carotid artery and vertebrobasilar artery) needs to be done If diabetic patient then Blood glucose Blood pressure measurement to rule out Hypertension Heart murmur it means there is vulvular heart disease which can cause emboli Echocardiogram to see an emboli Thoracic Aortic Aneurysm then CT scan chest

B. Investigation to make diagnosis: CT Scan of head 1. 2.

Ischaemic Haemorrhagic

General Management of cerebral vascular accident • • • •

If patient has symptoms of stroke do CT scan head to exclude haemorrhagic stroke. If no haemorrhagic stroke then give Aspirin 300mg stat If patient presents within 3 hours and no haemorrhagic stroke, arrange thrombolysis. If patient had symptoms of stroke, which have now resolved it means he had TIA - give aspirin 300mg orally, even before doing a CT scan because symptoms have resolved which suggests it is TIA.

Prophylaxis: Aspirin + dipyridamole If aspirin allergy substitute with clopidogrel

SPACE OCCUPYING LESION: Causes:

1. 2. 3. 4. 5. 6.

Tumour Abscess Haematoma Brain metastasis Aneurysm Granuloma

Symptoms:

• • • • • •

Usually in elderly patients Weight loss, anorexia Anaemia, tiredness Increased ICP: headache, vomiting and papilloedema Focal neurological signs (weakness in the limbs) Seizures

Investigations:

CT scan head

BRAIN TUMOUR:

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• • • • •

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Usually in elderly patients Symptoms are usually gradual onset Progressive worsening headache usually bilateral Adult onset seizure is always brain tumour until proven otherwise Headaches worse in the morning and on bending forward due to raised intracranial pressure

Treatment: 1.Dexamethasone if headaches or raised ICP to reduce oedema around tumour 2. surgery if localised tumour 3. Radiotherapy if metastasis but appropriate in that patient

MIGRAINE • • • • a. b. • •

Young, female patient typically Recurrent headaches: throbbing, pulsatile, unilateral Associated with nausea and vomiting Aura – can be sensory or visual Sensory aura usually tingling or numbness in upper limb Visual aura usually patient sees zig-zag lines but it can be any other form of visual loss) Aura usually lasts seconds to minutes and within 1 hour of aura headache follows there is usually family history

Investigations:

routine investigations, if diagnosis is not clear, to rule out other causes

Treatment: ACUTE = high dose aspirin 900mg or ketoprofin Prophylaxis:

1. 2. 3.

Beta-Blocker (Propranolol) Topiramate Amitryptalline

MYASTHENIA GRAVIS It is due to reduction in the number of nicotine AChR at neuromuscular junction. This is due to acetylcholine receptor antibodies formed against the acetylcholine receptor. There is abnormality of the thymus gland in 75% of the cases either in a form of hyperplasia or thymoma. It is an autoimmune condition. It is associated with other autoimmune conditions like SLE, Pernicious Anaemia, Grave’s disease, Rheumatoid Arthritis Symptoms: Painless muscle weakness which increases with exercise Generalised weakness Dysphagia, dysphonia, dysarthria, limb weakness There is fatiguability and weakness which worsens by the end of the day or whenever patient works hard. 5. Eye muscle weakness may present with diplopia 1. 2. 3. 4.

Investigation: 1. 2. 3.

Serum AChR antibodies are diagnostic of myasthenia gravis Tensilon (edrophonium) test diagnostic CT mediastinum to look for thymus gland

Treatment: 1. 2. 3. 4. 5. 6.

Cholinesterase inhibitor e.g. Pyridostigmine Steroid can be used if symptoms not adequately controlled by cholinesterase inhibitors Azathioprine if steroid is contraindicated Other immune suppressant e.g. ciclosporin, methotrexate may also be used Plasma exchange and immunoglobulin are used in patients with myasthenia crisis. Thymomectomy may be used in patients with AChR antibodies and under 45 years of age.

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BENIGN POSITIONAL VERTIGO This is characterized by recurrent episodes of dizziness provoked by quick change in position. Precipitating factors:

Trauma and viral illness.

This is a mechanical disorder due to movement of debris within the endolymph to the most dependent part of the canal during head movement. Typical symptoms are vertigo on turning over in bed, lying down or sitting up from supine position. Investigation:

Dix - Hallpike manoeuvre

Treatment: Epiley manoeuvre

Peripheral versus Central Nystagmus Peripheral Nystagmus:

• • • • •

Has fixed direction Last less than 60 second There is fatiguability i.e. lessing of symptoms with repetition Severe vertigo with nystagmus Inconsistent when trying to reproduce it

Central Nystagmus:

• • • • •

Consistent when trying to reproduce it Mild symptoms Marked nystagmus No fatiguability Symptoms are constant

HEADACHES 1.

CLUSTER HEADACHE:

Common in young middle aged men Usually unilateral severe headache, which radiates to the forehead Associated with redness of the eye and lacrimation. Severe headache which makes patient cry Headache occurs in clusters (comes and goes in periods e.g. 2 months of headaches at the same time and then 8 months of free headache and followed up by another period of headaches) this is why it is called cluster headache • Treatment is with high 100% oxygen and sumatriptan. • • • • •

1.

• • • • • •

GIANT CELL ARTERITIS: Typical age above 50 or elderly patients Common in women Unilateral headache on the temple areas Headache worse with combing hair, chewing (jaw claudication) Usually associated with weight loss, anorexia and weakness of the upper limbs In 25% it is associated with polymyalgia rheumatic which is an autoimmune condition mainly affecting the muscles especially those of the upper limb which make patient difficulty to stand up from the chair. Investigation:

1. 2.

Initial is ESR Definitive is temporal artery biopsy Management: If symptoms of GCA and ESR is raised then next step is treatment with IV methylprednisolone for 3 days followed by high dose oral prednisolone for 2 - 3 years i.e. long term.

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Definitive diagnosis of GCA is made by temporal artery biopsy within 3 days of provisional diagnosis.

1.

• • • •

TRIGEMINAL NEURALGIA: Usually electric shock like or knife like or stabbing pain in the face Usually in the distribution of the trigeminal nerve branch e.g. mandibular, maxillary or ophthalmic Pain can be triggered by shaving or chewing Facial pain runs up and down the face

Treatment: Anti-epileptic medication e.g. Carbamazepine, gabapentin 1.

• • • • • • •

1.

• • • • • • • • • •

1.

• • •

MIGRAINE: Common in young women. Unilateral pulsatile or throbbing headache Usually preceeded by visual or sensory aura Visual auras commonly are simply visual fortification or zig zag Sensory aura usually tingling and numbness in the hands Auras are followed by headache within 1 hour Headache usually associated with nausea and vomiting

ACUTE CLOSED ANGLE GLAUCOMA: Typically pain is in the eye with redness and lacrimation Usually associated with nausea, vomiting and loss of vision Unilateral headache Severe ocular pain Previous intermittent headache Usually there is family history Common in females Haloes around the light On examination there is corneal oedema (fine ground glass) and fixed dilated pupil oval shaped Raised intraocular pressure usually more than 40mmHg (normal IOP 45 years of age, after 3 miscarriages the risk of failure of the next pregnancy is 45%. (If patient has one miscarriage simply reassure). 5. Recurrent spontaneous miscarriage This is 3 or more consecutive miscarriage.

Anti phospholipid syndrome: suspect if any of the blood tests are positive. • Anti-phospholipid Antibodies, • Anti-cardiolipin Antibodies, • Lupus-anticoagulant antibodies

Most women with these antibodies have miscarriage in the 1st trimester (usually between 10 to 12 weeks). Treatment if any antibodies are positive: Aspirin 75 mg daily from the day of positive pregnancy test AND LMWH (enoxaparin/deltaparin) 40mg daily as soon as the fetal heart sound is heard (usually from the 5th week)

6. If Diabetic: Aim to control blood glucose. If on any other medication for diabetes it should be replaced by insulin and maintained throughout pregnancy (e.g. gliclazide, glibenclamide and metformin must be changed to insulin). DIAGNOSIS OF PREGNANCY 1. Common Symptoms:

Abdominal discomfort, nausea, vomiting and fatigue. 1. Pregnancy test: Urine pregnancy test

1. Dating of Pregnancy

1. From the LMP (last menstrual period) 2. Dating USS usually done at 12 weeks.

PRE-NATAL DIAGNOSIS Routine Pre-Natal Screening: Maternal serum screening is done in 15-18 weeks. It is usually offered to all women. i) Serum blood test 1. AFP (alpha fetal protein) 2. Beta HCG (human chorionic gonadotrophin) 3. Estriol Types of tests

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1. 2. 3.

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Double test = AFP + HCG Triple test = AFP + HCG + Estriol Quadruple = AFP + HCG + Estriol + Inhibin

Open neural tube defects (spina bifida) • Alpha-fetal protein (AFP) - highly increased • Human Chorionic Gonadotropin (HCG) - Normal • Estriol - Normal

Trisomy 21 (Down Syndrome) • AFP - Decreased • HCG - Increased • Estriol - Decreased

Trisomy 18 (Edward syndrome) • AFP - Decreased • HCG - Decreased • Estriol - Decreased

ii) Fetal Nuchal Scan Done at 8 – 12 weeks in which we look for nuchal fold thickness i.e. (accumulation of fluid in the neck of the baby) Abnormal Values for nuchal fold thickness • 8-12 weeks: >2.5mm • 12-16 weeks: ≥4mm • >16 weeks: ≥6mm

iii) USG Done at 18 – 22 weeks (It is an anomaly scan in which we usually look for structure abnormality)

Definitive Tests 1. Pre-Implantation diagnosis 2. Chorionic villus sampling 3. Amniocentesis

Indications for Definitive Tests: • • • • • • • •

Age > 35years Prior child with neural tube defect / chromosome defect Chromosomal abnormality in either of the parents Family history of abnormality Abnormal maternal serum tests Teratogen exposure Abnormal nuchal fold thickness Abnormal fetal structure survey (anomaly scan usually done at 12 weeks)

i. Pre-implantation genetic diagnosis ◦ Pre-implantation genetic diagnosis (PGD) is available to couples that are at risk of having a child with a specific genetic or chromosome disorder, such as cystic fibrosis, sickle cell disease or Huntington's disease etc. • Fertilisation is done in the laboratory. The embryos are tested for genetic abnormalities, 1 or 2 unaffected embryos are implanted into the uterus.

ii. Chorionic villous sampling (CVS) This is done at 10- 13 weeks) It is used if the screening test suggests aneuploidy (trisomies, cystic fibrosis, thalassemia, sickle cell disease). Other indications as above. Advantage: It is done early in pregnancy therefore it enables early termination of pregnancy if the woman decides not to continue with the pregnancy. Disadvantage: It has 1% risk of miscarriage and risk of transmitting infections like HIV and hepatitis to the child.

iii. Amniocentesis This is done at 15-18 weeks Indications • • • •

Screening test suggests aneuploidy Or it can be done for enzyme assays looking for inborn error metabolism (G6PD) DNA analysis for Cystic Fibrosis and Thalassemia Diagnosis of fetal infection (Cytomegalovirus, Toxoplasmosis) Advantage Carries low risk of miscarriage 0.1% Disadvantage Late identification of the affected fetus leads to late termination.

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ANTE-NATAL CARE Consist of 1st, 2nd and 3rd trimester visits. Antenatal care starts once the pregnancy is confirmed. Routine tests (these tests are offered to all women in the UK) • FBC • Blood Group • Antibody Screen (ABO & Rh) to assess the risk of rhesus incompatibility • Routine infection screen (rubella, syphilis, hepatitis, HIV)

Specific blood tests: • Afro-Caribbean origin = sickle cell test • Screening for Thalassaemia (Cyprus, Eastern Mediterranean, Middle-East, South-East Asia, Indian subcontinent).

PREGNANCY FIRST TRIMESTER COMPLICATIONS

a) Hyper-emesis Gravidarum: Excessive vomiting or severe morning sickness 1ST Trimester • • • • • •

Vomiting, can cause weight loss Muscle wasting Dehydration Inability to swallow saliva Thirst Tired due to dehydration

Investigations U&E (Na, Urea and Creatinine will be increased LFT, FBC, USGto exclude multiple pregnancy & molar pregnancy . Treatment 1) Admit + IV fluids ( if cannot tolerate oral fluids) + check blood + keep NBM for 24 hrs then introduce some light diet. 2) Antiemetic eg. IM Cyclizine, metoclopramide, prochlorperazine, promethazine, chlorpromazine, domperidone and ondansetron 3) Thiamine should be prescribed routinely either orally or IV 4) If vomiting doesn’t stop with antiemetics then give steroids.

b) Recurrent Miscarriages: This is 3 or more consecutive miscarriage Causes 1.

Anti-Phospholipid syndrome

Treatment for anti phosphoslipid syndrome: • Aspirin 75 mg from day of +ve pregnancy test • LMWH like enoxaparin as soon as fetal heart sound heard or from 5 weeks.

2.

Genetic causes like chromosome translocation or Fetal Chromosomal Abnormality

Treatment if family Hx. positive: Refer for genetic test and counseling 3.

Fibroids: Common in Afro-Caribbean women. It can be so big that it can distort the uterine and a myomectomy may be needed.

4. Thrombophilia is inherited and causes recurrent miscarriage. Rx is with LMWH (enoxaparin). Patient usuallypresents with thrombosis, DVT and PE. 5. Uterine abnormalities e.g. that of uterine septum usually causes miscarriages in the 2nd trimester. 6.

Infection like bacterial vaginosis

7.

Endocrine causes like PCOS

c) Infection Group B Streptococcal infection (GBS) • Asymptomatic in pregnant women. • Diagnosis is culture from endocervical swab. If that option is not available then choose lower vaginal swab, if that is not available choose high vaginal swab or perianal swab • Up to 70% of all children born from infected GBS mothers are also colonized at delivery but only 1% develop infection • GBS can cause Pneumonia, Septicaemia , Meningitis

Prevention: Antibiotics are given to mothers during delivery if they are colonized with GBS or if mothers have previous Hx. of GBS infection Treatments: Intravenous Benzyl penicillin

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a. Abortion (Termination of pregnancy) Under UK laws no one has to have abortion and no one has to do one, unless there are medical or social reasons like risk to mothers life if the pregnancy continues. Methods of abortion: • < 7 wks – medical • 7-15wks – medical or surgical • >15 wks – medical

Medical Treatment • Mifepristone orally and then gemeprost per vagina 36-48 hours later

OR • Mifeprestone orally followed by misoprostol per vagina 36-48 hours later

NB. Add second medication only if abortion not completed

Surgical Treatment is by D& C (dilatation and curettage)

e) Bleeding in 1st trimester of pregnancy Commonly associated with 1. Miscarriage 2. Ectopic pregnancy 3. Gestational trophoblastic disease

Miscarriage: This is a spontaneous abortion. It is defined as expulsion or removal of the embryo or fetus at a stage of pregnancy when it is incapable of independent survival. NB: This is loss of pregnancy BEFORE 24 weeks (AFTER 24 weeks it is called STILL BIRTH) Majority of miscarriages occur between 10-12 weeks

Management: • • • •

Send to early pregnancy assessment unit (EPAU) Transvaginal Ultrasound scan Serum HCG Anti D prophylaxis 1. 2. 3.

Non-sensitised with rhesus –ve factor and12 weeks gestation who are bleeding If any medical or surgical intervention has been used.

TYPES OF MISCARRIAGE i) Threatened miscarriage • • • •

Bleeding per vagina With or without abdominal pain Closed cervical os USS shows intrauterine gestation sac, fetal poles, fetal heart activity

Management: give anti D if > 12 weeks gestation or if having heavy bleeding.

ii) Complete abortion • • • • •

Bleeding per vaginal Abdominal pain Closed cervix USS shows empty uterus Endometrial thickening < 15 mm

Management: Anti-D if >12 weeks or heavy bleeding or if Rh-ve. Monitor serum HCG (human chorionic gonadotropin)

iii) Incomplete abortion • • • • •

Bleeding per vaginal - usually there is passing of large clots With or without abdominal pain Cervix open on PV examination USS shows heterogeneous tissue +/- gestational sac No fetal activity

Management: Medical or expectant management , Anti D if > 12 weeks

iv) Missed miscarriage (Fetus dies but is retained in the uterus)

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• • • • • •

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+/- bleeding +/- abdominal pain +/- loss of pregnancy symptoms USS shows no fetal activity (but the fetus is in the uterus) No fetal pole, yolk sac Os closed

Management: Surgical or medical, Anti – D if > 12 weeks.

v) Inevitable abortion (miscarriage) • • • • •

Bleeding per vaginal +/- abdominal pain Open cervix USS shows +/- gestational sac , +/- fetal pole Positive fetal heart activity

Management: Surgical/medical/expectant Most appropriate treatment is expectant management Give Anti-D if >12 weeks Expectant Management: • Highly effective in incomplete miscarriage • If expectant management is unsuccessful then offer surgery • Warn about pain and increased bleeding

Medical Management: • Prostaglandin analogues

e.g. misoprostol or gemeprost either P/O or P/V. • Bleeding can take up to 3 weeks • 24hrs telephone advice should be available admission

Surgical Management: • Evacuation of retained product of conception • Suction and curettage may be used • Indications: Excessive bleeding, inevitable abortion, missed miscarriage, patient request

Complications of Surgical Management 1. Infection 2. Haemorrhage 3. Uterine perforation 4. Cervical tears 5. Intra uterine adhesions (Asherman’s syndrome) This can lead to infertility.

Ectopic Pregnancy: This is implantation of the products of conception outside the uterus Symptoms • • • • • •

Amenorrhea of typically 6-8weeks Lower abdominal pain Shoulder tip pain Adnexal tenderness Cervical excitation and tenderness PV bleeding

Investigations • • • •

Urine Pregnancy Test TV USS scan Serum pregnancy test (beta HCG) Diagnostic laparoscopy

Management Depends on clinical picture 1. If patient collapsed / in shock = do pregnancy test. If positive, perform URGENT LAPAROTOMY.

2. If pregnancy test positive with abdominal signs of ectopic pregnancy (shoulder tip pain, pelvic tenderness, cervical excitation test) , do Transvaginal ultrasound scan- If it shows an empty uterus perform Diagnostic laparoscopy. 3. If pregnancy test positive but Uterus empty on TV scan and no abdominal signs do quantitative serum HCG A. If serum HCG > 1000 IU following a TV Ultrasound scan or if > 6500 IU following transabdominal scan perform Diagnostic laparoscopy

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A. If less than the above figures, then recheck beta HCG in 48hrs.

• Beta HCG should fall to less than half the baseline value every 48 hours.

• If beta HCG not less than half the baseline value or steady or only slightly reduced perform Diagnostic laparoscopy.

• If falling rapidly it means the pregnancy is aborting. If patient is well then only expectant management is needed. Repeat HCG to ensure levels are falling.

NB : IF SYMPTOMS DEVELOP AT ANYTIME THEN DO LAPAROSCOPY Management: • Laparoscopy is preferred • Laparotomy is preferred only if patient is in shock or collapsed

Procedure: Ectopic in fallopian tube is treated either by Salpingotomy or Salpingectomy. Gestational Trophoblastic Disease a. Hydatidiform mole (premalignant) • • • • •

Large for dates Exaggerated symptoms of pregnancy Hyperemesis Gravidarum due to markedly increased beta HCG Hyperthyroidism “Snowstorm” appearance on ultrasound

Management: • Suction curettage is the method of choice of evacuation • Give Anti-D prophylaxis • Monitor Beta HCG after evacuation every 2 weeks until normal. After Beta HCG is normal, monitor monthly for up to 6 months. • Measure Beta HCG 6-8 weeks after any future pregnancy regardless of outcome

a. Gestational trophoblastic neoplasia/Choriocarcinoma (malignant) • Usually follows a molar pregnancy but can follow a normal pregnancy, ectopic pregnancy or abortion • Should always be considered when a patient has continued vaginal bleeding after the end of a pregnancy. • Should also be considered in any woman developing acute respiratory or neurological symptoms after any pregnancy (due to metastasis)

Management: Chemotherapy

2. SECOND TRIMESTER COMPLICATIONS a. Pregnancy Induced Hypertension (PIH) • Defined as hypertension in the 2nd trimester of pregnancy in the absence of proteinuria or other markers of preeclampsia. • PIH includes risk of developing pre-eclampsia • Delivery should be aimed at the time of expected date of delivery.

Treatment: i) Methyldopa ii) Labetalol iii) Nifedipine

a. Pre-Eclampsia • BP ≥140/90 and 300 mg proteinuria in 24 hour urine collection • In women who are already hypertensive a rise of BP ≥ 30 mmhg systolic or ≥ 15 mmhg of diastolic is used

Risk factors • • • •

Previous severe or early pre-eclampsia Age > 40 years Family history of pre-eclampsia DM , HTN , Renal diseases

Signs & Symptoms • • • • • • •

Headache Visual disturbances Epigastric or RUQ pain Nausea & vomiting Rapid oedema especially of the face BP ≥ 140 /90 or In severe pre-eclampsia BP is ≥ 170 /110

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• Proteinuria > 300 mg / 24hrs • Confusion

Investigation: To rule out HELLP Syndrome • FBC - Thrombocytopenia & Anaemia • Coagulation profile – PT & APTT are prolonged • Biochemistry – increased Urea & Creatinine.

1. Mild to Moderate Pre-Eclampsia Definition: BP < 160 systolic and < 110 diastolic with significant proteinuria and no maternal complication Management • • • • • • •

If significant proteinuria then ADMIT {i.e + + proteinuria or > 300 mg proteinuria /24hrs} 4 hourly BP Cardiotocography to monitor for fetal distress Daily urinalysis to check for proteinuria 24hr urine collection for proteinuria Regular USG assessment every 2 weeks to monitor for fetal retardation IF > 160 SYSTOLIC OR >110 DIASTOLIC START ANTI –HYPERTENSIVE

2. Severe Pre-Eclampsia Definition: BP ≥ 160 systolic or ≥ 110 diastolic in the presence of significant proteinuria (≥ 1g /24hrs or >++ on dipstick ) or if maternal complications occur . Management • • • • • •

Anti hypertensive to bring BP down to < 160 systolic and < 110 diastolic. Hydralazine intravenously is the 1st choice Labetalol Give MgSO4 to prevent eclampsia CTG & USG to monitor to baby If less than 34 weeks gestation give steroids to help production of surfactant.

Complications of Pre-eclampsia 1. Eclampsia 2. HELLP syndrome – Haemolysis, Elevated Liver enzymes , Low Platelets 3. DIC 4. Renal failure 5. Placental abruption

Indications for Immediate Delivery in Pre Eclampsia: 1. Worsening thrombocytopenia or coagulation profile 2. Worsening renal or liver functions 3. HELLP syndrome 4. Eclampsia 5. Fetal distress-as shown by CTG 6. Severe maternal symptoms

A. Eclampsia

Definition: Symptoms of Pre eclampsia + seizure = eclampsia HELLP syndrome is regarded as a variant of severe pre – eclampsia. NB. If a woman has a fit a few days after delivery, it is always eclampsia until proven otherwise because eclampsia can happen in the post partum period.

Management: • ABC • MgS04 intravenous bolus 4g, then 1 g intravenous infusion for 24 hours and if seizure recurs give intravenous bolus. • Monitor BP, pulse , RR & O2 saturation every 15 minutes • If BP > 160/110 give anti hypertensive (Hydralazine , labetalol , nifedipine) • CTG to monitor the baby • Deliver the baby once the patience is stable, delivery is by caesarean section usually but if appropriate then Per Vaginal.

NB. If patient has been given Magnesium sulphate and suffered another fit, repeat Magnesium sulphate.

3. THIRD TRIMESTER COMPLICATIONS

Antepartum Haemorrhage in the 3rd trimester Common Causes i. Placenta Praevia ii. Placenta Abruption

i.Placenta Previa The placenta is inserted wholly or in part into the lower segment of the uterus. Types:

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• Placenta major - the placenta completely covers the cervical os • Placenta minor - the placenta is located close to the cervical os or cover it partially

Presentation: Bright red painless bleeding per vagina. Investigation: Transvaginal USS is more accurate than transabdominal Management 1. If major Placenta Praevia and bleeding – Admit patient 2. If placenta edge is < 2cm from the internal Os then elective caesarean is the mode of delivery

ii. Placenta Abruption This is when the placenta separates from the uterus before delivery of the fetus. Blood accumulates behind the placenta in the uterine cavity or is lost through the cervix.

Presentation: Dark coloured blood per vagina with sudden onset, severe, constant abdominal pain with rigid abdomen. Investigation: Diagnosis is clinical but ultrasound is done to exclude PP and to check the baby. Management 1. 2. 3. 4.

Admit Check the wellbeing of the baby with cardiotography (CTG) and USS. If fetal distress or maternal compromise resuscitate and deliver now (caesarean). If no fetal distress deliver by term.

Distinguishing Placental Abruption from Placental Praevia Placental abruption • • • • •

Shock is out of proportion from visible blood loss Constant pain Tender tense uterus Fetal heart sounds absent/distressed Coagulation problems like DIC Placenta Praevia

• • • • •

Shock in proportion with visible blood loss No pain Non tender uterus Normal fetal heart sounds Coagulation problems are rare

MEDICAL PROBLEMS IN PREGNANCY a. Diabetes • • • • • • •

Avoid unplanned pregnancy Monitor Hba , c 1 month + 12 give 0.5ml 2. Age 6 years-12 years give 0.3ml 3. Age 60 – diagnostic.

Complications: Common complication is bronchiectasis which is dilatation of the bronchi due to recurrent chest infection. Usually develops but the age of 20 years.

Management: 1. Symptomatic management 2. Physiotherapy 3. Antibiotics if there is chest infection

Asthma Chronic allergic reaction characterised by reversible airway, obstruction, wheeze, cough and dyspnoea. Triggers: pollen, dust, feather, fur, exercise, infection. Prophylaxis 1. Avoid triggers 2. Use sodium chromoglycate in exercise induced asthma or pre-exercise bronchodilator (salbutamol)

Management: 1. Stable patient: Goes to GP or outpatient department (salbutamol) 2. Unstable patient: Patients come to A&E and have severe symptoms

A. Stable patient

Step 1: Occasional short acting B agonist inhaler e.g salbutamol as required. If needed > 2/week or (night symptoms) or if getting exacebationmove to next step. 2

Step 2: Add regular Inhaled Steroid: Therefore at this stage child will be taking salbutamol as required and inhaled steroid e.g. beclomethsone 400 mg. If not effective then increase up to 800 mg.

Step 3: Check diagnosis, check technique (use the spacer with a mask). Add 1 dose montelucast (leucotriene antagonist) in the evening. If 2-5 years add leukotriene antagonist (e. g. montelucast), fulmeterolol. If 5 years add Long acting – agonist e.g. salmeterolol. At this stage if not getting any benefit from long acting beta-agonist them discontinue it. But if it has added some benefit then continue it.

Step 4: Increased inhaled steroid up to maximum dose (e.g Beclomethasone 800 μg --- 1000 μg). If child develops oral candida reduce the dose. At this stage also consider leukotriene antagonist if not already used or modified long acting beta agonist or aminophylline

Step 5: Add prednisolone – oral

A. Unstable patient = Acute exacerbation of asthma.

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Patients with acute problems usually go the accident and emergency department a. Mild to moderate asthma (able to talk, Pulse < 125, PEFR > 35% of the predicted value. Oxygen > 92%.

Treatment: 1. Oxygen 2. Nebulised salbutamol or terbutaline 3. Prednisolone.

a. Severe asthma ( can not speak in complete sentences in one breathor child too breathless to speak, PEFR 35%-50%, Oxygen saturation < 92%)

Treatment: 1. Oxygen - high flow 15L/min or 100% 2. Neb salbutamol ± IV salbutamol 3. Oral Prednisolone or IV hydrocortisone 4. IV MgSO

4

5. Aminophyline

a. Life threatening asthma: (Silent chest, cyanosis, hypotension, bradycardia, agitation, reduced consciousness, saturations < 92%)

1. Oxygen - high flow 15L/min or 100% oxygen 2. Nebulised salbutamol ± IV salbutamol 3. Oral prednisolone or IV hydrocortisone 4. IV MgSO

4

5. Aminophylline

N.B: Intravenous Salbutamol can be used if patient is not able to nebulise for e.g. if someone is vomiting.

Congenital Heart Disease

A. Cyanotic • Tetralogy of Fallot • Right ventricular hypertrophy • Pulmonary stenosis • Ventricular Septal Defect (VSD) • Overriding aorta • Chest X-Ray shows booth shaped heart • Transposition of the great arteries, Chest X-Ray shows egg shaped heart

B. Non Cyanotic 1. VSD = loud pan systolic murmur (harsh) 2. Atrial Septal Defect (ASD) = systolic murmur in the upper left sternal edge 3. Patent ductus arteriosus (PDA) = systolic continuous machinery murmur on the pulmonary area 4. Coarctation of aorta = unpalpable or weak femoral pulses 5. Aortic Stenosis = crescendo-decrescendo systolic ejection murmur

Convulsing child

Causes

1. Epilepsy 2. Febrile convulsion (Fits caused by high temperature) 3. Brain tumours

Management:

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1. The most appropriate treatment is IV Lorazepam. 2. If the patient is not responding, give another dose of IV Lorazepam. 3. If the patient is still having seizures, load with phenytoin 4. If the patient is still convulsing, give phenobarbital 5. If the seizure is still ongoing, put patient under general anaesthesia and intubate.

NB. If no IV access, give per rectal diazepam

Vomiting in infancy

1. Meningitis = rash, photophobia, fever, drowsy headache 2. Pyloric stenosis = projectile vomiting • No bile in vomiting (Investigation: Ultrasound Scan) • No diarrhoea • Dehydrated and hungry child [6 week old baby] – olive shaped mass in epigastrium 1. GERD = vomiting usually occurs after feeding, it is usually reduced when the child sits up 2. Overfeeding = also after feeding and child is described as greedy baby 3. UTI = fever, vomiting, failure to thrive

N.B. In both GERD & overfeeding, vomiting occurs after feeding.

1. Gastroenteritis: Commonest cause of diarrhoea and vomiting is Rotavirus infection a. Viral b. Bacterial: Fever, bloody diarrhoea, abdominal pain, vomiting

Investigations: = U&E to check for dehydration Management: Rehydration with Oral Rehydration Salts (ORS) 60 mmol/L of Sodium

Childhood jaundice

Differential Diagnosis

1. Physiological: 24hours - 14 days 2. Breast milk jaundice 3. Haemolytic, sepsis 4. Urinary Tract Infection

5. Hypothyroidism 6. Biliary atresia 7. Galactosemia 8. Hepatitis A 9. α- antitrypsin 10. Prematurity 11. Rhesus incompatibility 12. ABO incompatibility 13. Bruising

Physiological jaundice • Jaundice in the neonatal period is very common and is usually due to a physiological immaturity. It is self-limiting as the liver matures over the first week. Nearly all preterm infants become jaundiced in the first few days of life, due to the immature hepatocytes. • Low liver enzyme activity • Breakdown of fetal haemoglobin

Breast milk jaundice

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• This is persistent jaundice in an otherwise well, breast-fed infant. This is due to the inhibition of liver conjugation enzymes. Split bilirubin should be measured (conjugated & unconjugated) to exclude conjugated hyperbilirubinaemia. Normally manifests itself by day 4-7. • Well baby who is breast-fed. • Jaundice develops in second week.

Hypothyroidism • May be associated with pituitary disease

Biliary atresia • Present 4-6 weeks after birth • Present in obstructive jaundice • A conjugated hyperbilirubinaemia develops over a period of weeks. Stools become clay coloured i.e pale stools and dark urine • Persistent jaundice with rising conjugated fraction • Pale, chalky stools • Requires urgent referral for assessment, diagnostic isotope scan and surgical correction.

Prematurity – Pre-term born babies • Immature liver enzymes

Rhesus incompatibilty • Usually develops on the first day of life • If mother is Rh negative and baby Rh positive, the maternal IgG can cause haemolysis • Sensitization occurs in earlier pregnancies • If severe can cause hydrops in utero • Coombs’ test positive, high unconjugated bilirubin

ABO incompatibility – Autoimmune – Coombs’ positive • Usually milder than rhesus

Bruising • Skin or scalp bruising from traumatic delivery is broken down into bilirubin

Key points • Mild jaundice is extremely common in newborn infants, especially preterm ones. • Jaundice within the first 24 hours or lasting beyond 2 weeks needs investigation. • Phototherapy and occasionally exchange transfusion are used to treat significant jaundice. • Biliary atresia causes an obstructive persistent jaundice with pale stools. Early treatment is essential. • Conjugated hyperbilirubinaemia is always abnormal. Exclude biliary atresaia.

N.B. • < 24 hours = pathological • > 24 hours = usually physiological

Investigations – Serum bilirubin

Routine Paediatric Immunisations

• 2 months - 5 in 1 (DTaP/IPV/Hib), PCV, Rotavirus (by mouth) • 3 months - 5 in 1 (DTaP/IPV/Hib), MenC, Rotavirus • 4 months - 5 in 1 (DTaP/IPV/Hib), PCV • 12 - 13 months - Hib/MenC, PCV, MMR • 2 and 3 years - Flu nasal spray • Pre school (3 years 4 months) - DTaP/IPV, MMR • Girls 12-13 years - HPV • Around 14 years - Td/iPV, MenC

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Key: • DTaP - Diphtheria, Tetanus, acellular Pertussis (in thigh) • IPV - Inactivated Polio Virus • Hib - Haemophilus influenza type b • PCV - Pneumococcal Conjugate Vaccine (in thigh) • Men C - Meningococcal group C • MMR - Measles, Mumps, Rubella (upper arm/thigh) • HPV - Human Papillomavirus (upper arm) • Td - Tetanus, diptheria (upper arm)

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• ◦ ◦ ◦ ◦ • +44 0208 9800 039 +44 0794 0433 068 • • • •

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Psychiatry

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PSYCHIATRY NOTES

MENTAL STATE EXAMINATION

I. APPEARANCE AND BEHAVIOUR • State and colour of clothes • Eye contact (Poor eye contact in depression) • Tearful (Depression) • Down cast gaze • Agitation(seen in depressive illness, anxiety, psychosis) • Tremor, Fidgeting • Distracted • Visual scanning (for danger)

II. MOOD AND AFFECT The patient has an emotion and feeling, tells the doctor their mood and the doctor observes the patient affect Affect is the mood by appearance of the patient as judged by the doctor Mood Alteration Persistent change in mood Fluctuating or labile mood Inconsistent or incongruent mood

A persistent change in mood 1. Depression: • Low mood • Feeling sad • Tearful & low in spirits • Feeling guilty & low confidence level • Anhedonia – loss of interest in daily activities • Loss of appetite & weight • Loss of libido

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2. Anxiety: A feeling of constant inappropriate or excessive worry, fear or tension. Common in young women 3. Irritability: Temper or impatient 4. Elation: Feeling of high spirits e.g. mania 5. Blunting of affect: Total absence of emotion, seen more commonly in chronic schizophrenia

Fluctuating or labile mood This is when different emotions rapidly follow one another so that a patient is crying one moment and laughing the next.

Inconsistent or incongruous mood This occurs when emotional expression fails to match thoughts and actions e.g. Patient may laugh when describing the death of a relative

SPEECH Disorders of stream of thought 1. Pressure of speech: Can be recognized by loudness, rapidity and difficulty in interrupting speech e.g. mania 2. Poverty of speech: Absence of any thought and patient report their mind to be empty e.g. in schizophrenia 3. Thought block: Speech is normal initially and then it stops suddenly Occurs in schizophrenia i.e. there is an abrupt(sudden) and complete interruption of the stream of thought, so the mind goes blank

Disorders of form of thought

1. Flight of ideas Patient’s thoughts rapidly jump from one topic to the next, such that one train of thought is not completed This is characteristic of mania and is often accompanied by pressure of speech 2. Preservation: persistent and inappropriate repetition of same thoughts or action. Occurs in frontal lobe lesions e.g. If you ask patient to say No Ifs ands or buts, he will say No ifs ifs ifs…… 3. Loosening of associations: loss of normal structure of thinking It is usually difficult to understand what the patient is speaking 4. Thought broadcasting A feeling as if other people are hearing or understanding their thoughts despite not telling people what they are thinking. E.g. schizophrenia 5. Thought insertion Feeling that someone is putting thoughts into their mind. Patient feels that the thoughts in his mind are not his/her. E.g. schizophrenia 6. Thought withdrawal Feeling that someone is taking my thoughts away or stealing of thoughts 4, 5 and 6 are the 3 factor’s which indicate schizophrenia

IV. THOUGHT CONTENT 1. An obsessional rumination: is a recurrent, persistent thought, impulse, image or musical theme that enters the mind despite individual’s effort to resist it. E.g. Obsessive Compulsive Disorders 2. Compulsion: is a repetitive and seemingly purposeful action performed in a stereotyped way which is called a compulsive ritual. E.g. Obsessive Compulsive Disorder

V. INSIGHT Is the awareness of the patient that he or she is unwell or has a problem.

ABNORMAL BELIEFS these are called delusions A delusion is an abnormal belief that is held with absolute conviction Not amenable to reason or modifiable by experience Usually false Not shared by those of common social or cultural background

ABNORMAL PERCEPTION 1. Illusion: This is the distortion or misinterpretation of external stimuli or real things e.g. see a tree as if it’s a person

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2. Hallucination: hearing or seeing things which are not there and without any stimuli. It is a false perception and not distortion. • Hypnogogic Hallucinations: Episodes of seeing or hearing things as one is falling asleep. These dreams can be frightening and one can often cause a sudden jerk and arousal just before the sleep. It is associated with narcolepsy. • Hypnopompic Hallucinations: Episodes of seeing, hearing or feeling things while getting up from sleep. E.g. Narcolepsy • Auditory Hallucinations • Visual Hallucinations e.g. schizophrenia, substance abuse- PCP or cocaine • Tactile Hallucinations e.g. small insects crawling on skin in chronic alcoholics or alcohol abuse • Gustatory Hallucinations • Olfactory Hallucinations • Third Person Hallucination (Usually auditory-Running commentary that he is an evil person and ants to kill me)

3. Pseudo or False hallucinations: usually auditory e.g. hear a voice in my head speaking to me. Patient have insight to the problem 4. Derealization: unpleasant feeling that he external environment has become unreal i.e. patient feel like that they are in a dream like state 5. Depersonalization: change in self awareness such that a person feels unreal or detached from their body 6. Déjà vu: a sudden familiarity with the situation or event as having been encountered before when it is in fact new. 7. Jamais vu: Failure to recognise an event or situation which was encountered before.

FUNCTIONAL DISORDERS 1. CHRONIC FATIGUE SYNDROME • This is when a person feels tired, fatigued all the time • All investigations are normal • Fatigue and tiredness does not improve with rest • No structural abnormalities found

Management: Education and reassurance, Education about appropriate rest and activity, CBT, Graded Exercise Program, relaxation therapies- yoga, meditation. Referral to psychiatrist and psychologist 2. FIBROMYALGIA (Chronic widespread pain) • This a functional widespread pain all over the body • All investigations are normal

3. IRRITABLE BOWEL SYNDROME • Functional disorder • Presents as abdominal pain which is usually relieved by passing flatus or stools • Diarrhea, bloating, constipation • All investigations are normal • It is a diagnosis of exclusion • No PR bleed • No night symptoms • No weight loss

Management: Education and symptomatic treatment

4. PREMENSTRUAL SYNDROME • Physical and psychological symptoms that regularly occur during the premenstrual phase and diminishes soon after the period starts • Cause is likely to be hormonal • Abdominal pain, Irritability, Low mood, Bloating

SOMATOFORM DISORDERS

1. SOMATIZATION DISORDER • This is multiple, recurrent, medically unexplained symptoms, usually starting early in life. Usually patient presents with one symptom at a time. • Nausea, Vomiting, Abdomen pain • Neck pain, Back pain, Headache • Etiology is unknown • Investigations are normal

2. HYPOCHONDRIASIS

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• Preoccupation with assumed serious diseases. • Commonly patient believes they are suffering from cancer or HIV even after repeated reassurance with normal investigations for symptoms and they repeatedly request investigations.

NB: Management of somatoform disorders is reassurance and education, Referral to psychologist. DISSOCIATIVE DISORDERS (Conversion) • Also known as hysteria. • It is a condition where there is a profound loss of awareness or cognitive ability. • E.g. Amnesia- loss of memory • E.g. Pseudo-seizure (Psychogenic non epileptic seizures): Seizure like activity resembling epileptic fit but without any electrical discharges associated with epilepsy and the patient is not hurt during this seizure and usually tries to resist any attempt to change his posture by other people. Long-term video EEG & Serum prolactin is usually done to distinguish between true seizure and pseudo-seizure.

MOOD (Affective disorders) Depressive disorders A. Unipolar: Depression occurring on it’s own. B. Bipolar: Depression alternating with mania.

Bipolar affective disorder A. DEPRESSION 1. Low mood 2. Low energy level 3. Feels sad 4. Anhedonia – loss of interest in daily activities 5. Early morning waking 6. Loss of appetite 7. Feeling guilty 8. Reduced self esteem 9. Thoughts of self-harm 10. Fatigability – feeling tired 11. Loss of libido

B. DYSTHYMIA It is characterized by the mild depressive illness that lasts intermittently more than 2 years.

C. SEASONAL AFFECTIVE DISORDER It is characterized by the recurrent episodes of depressive illness occurring during the winter months. It occurs annually usually in winters. • Atypical symptoms • Low mood, anhedonia • Excessive sleep • Increased appetite and weight gain

Management: Light therapy, Pscho-therapy and antidepressants.

D. POST NATAL DEPRESSION • Occurs after delivery • Poor sleep, low confidence, anhedonia • Loss of appetite & weight • Feeling that she is not capable of looking after her child • Guilt feeling that she is not a good mother • Tearful, Anxiety • Occurs in the first 3 months after delivery • Mother feels as if someone/partner wants to harm her baby

E. BABY BLUES • Occurs in 50% women after giving birth • Normal phenomena and resolves within a few days usually 3-4 days • Poor sleep, anxiety, irritability, tearful, crying for no reason

Management: Family support & Reassurance

F. POST NATAL PSYCHOSIS • Usually occurs within 2 weeks after delivery • Usually starts with post-natal depression • Delusional ideas that the baby is deformed, evil or otherwise affected in some way and she has intent to kill the baby, evils or self harm

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G. BIPOLAR AFFECTIVE DISORDER Mood swings of mania and depression

Treatment of depressive illness 1. SSRI: Selective Serotonin Re-uptake Inhibitors: First choice of treatment • Citalopram- Preferred in IHD • Escitalopram • Fluoxetine • Paroxetine

2. Tricyclic Antidepressant (TCA) • Amitryptilline • Dosulepin • Lofepramine, Trazodone

Contraindication: in Ischaemic Heart Disease (IHD) and Glaucoma Side Effect’s: • Arrythmia’s • Dry Mouth • Constipation • Raised Intra-ocular pressure- leads to Glaucoma

3. Other Anti depressants • Mirtazapine • Venlafaxine • Reboxetine

4. Monoamine oxidase inhibitors (MAOI) • Phenelzine

NB: 1. Depression with obesity=fluoxetine (It helps without weight loss) 2. Depression with sexual dysfunction=mirtazapine 3. Post stroke depression use nortriptyline (TCA) 4. Depression with obsessive compulsive disorder=clomipramine (TCA) 5. Depression with ischemic heart disease=SSRI e. g citalopram NON-MEDICAL TREATMENT a. Electroconvulsive therapy (ECT) Indications: 1. Refusing to eat and drink and their weight is dangerously going low 2. Dangerously suicidal (Patient’s looking for every opportunity to kill themselves) 3. Psychotic symptoms 4. Depression not responding to anti-depressants 5. Depression with Psychosis b. Cognitive Behavior therapy Good for mild to moderate depression. It is as effective as medical treatment. Good for anxiety disorder It involves identification of abnormal thinking that keeps triggering depressive, anxiety or any other symptoms and tries to fix or change it. E.g. Depression, OCD, PTSD c. Behavior therapy Based on learning theory Works as desensitization e.g. in OCD, phobia (arachnophobia- fear of spiders, agoraphobia- fear of open spaces, claustrophobia- fear of closed spaces) d. Interpersonal psychotherapy Used for depression and eating disorder especially depression triggered by personal relationship

e. Couple therapy When a patient with depression is having problems in relationship like sexual, emotional etc. f. Family therapy If family is supportive – educate the family about the condition and the members of the family g. Supportive therapy It is similar to counseling. E.g. Bereavement, baby blues h. Group therapy Where a problem involves a group of people e.g. drug abuse

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I. Exposure and Response Prevention Therapy Used in OCD & phobia’s SEROTONIN SYNDROME • Toxic hyper-serotonergic state • Occurs when SSRI and MAOIs are used together or overdose of SSRI’s or when 2 SSRI’s are started together. Symptoms: • Agitation • Confusion • Tremor • Diarrhea • Tachycardia • Hypertension

II. MANIA AND HYPOMANIA Elevated mood: characterized by euphoria, overactivity and disinhibition

Hypomania: is mild form of mania, it lasts shorter time and less severe Mania: almost always occurs as bipolar affective disorder Clinical features of Mania • Elevated mood • Fast pressurized speech, flight of ideas • Excessive energy, anhedonia, self confident, Over-spending, delusion of wealth • Delusion of Grandiose • Delusion of Control • Dis-inhibition • Hallucination

Treatment of MANIA ACUTE TREATMENT 1. Lithium is the first choice 2. Antipsychotic is 2nd line eg. Halperidol or chlorpromazine

PROPHYLAXIS 1. Lithium is the first choice 2. If not responding to lithium then use anti convulsants e.g. Carbamazepine

Monitor patients on Lithium with Thyroid functions tests and U & Es

Lithium adverse affects: • Can cause nephrogenic diabetes insipidus which presents with polyuria, polydipsia. • Hypothyroidism • Nausea • Tremor • Weight gain

At therapeutic levels lithium has the following side effects

ANXIETY DISORDERS

1. Generalized anxiety disorder Patient is worried about different number of events every day. Almost everything triggers the anxiety.

2. Mixed anxiety and depressive disorders There is equal amount of anxiety and depression • Palpitation & chest pain • Excessive worries • Low mood • Poor sleep & guilt feeling • Reduced appetite

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3. Panic disorder or Anxiety attack • There is hyperventilation (SOB) difficult to take a deep breath • Chest pain (all over the chest) • Choking sensation • Palpitation, sweating • Perioral paresthesia & Tingling and numbness in the hands due to hyperventilation and CO2 washout leading to low ionic calcium. • Patient has belief of catastrophic illness e.g. MI or stroke • Feeling of Impending doom or feeling as if having a heart attack or going to die. • Feeling of butterfly’s in tummy

Management • Rebreathing bag • Reassurance • Relaxation therapy • Beta-blocker can be used for upcoming stressful event e.g. an exam or a job interview but is not used acute attack of panic attack. In acute attack use re-breathing bag. • Anxiolytics: E.g. Diazepam- If having severe symptoms

PHOBIA DISORDERS 1. Agarophobia: translated as fear of the market place, fear of going out in open places. As soon as patient is out, starts to have panic attack. e. g shops, markets 2. Social phobia: Fear to socialize with other e.g. Meetings, Parties, Crowds and with normal life.

Simple phobias Arachnophobia: Fear of spiders particularly in women. Treatment: Exposure and response prevention therapy, Desensitization, Behavioral therapy. Treatment of anxiety disorder 1. Relaxation therapy: If symptoms have resolved 2. Behavior therapy: Graded exposure called systemic desensitization – first choice treatment for phobias. 3. CBT: Best Rx for panic disorder, endogenous phobia and anxiety disorder 4. Drugs: Anxiolytic: e.g. Benzodiazepine

ACUTE STRESS AND ADJUSTMENT DISORDERS 1. Acute stress disorder • Occur in individual without psychiatric illness, in response to exceptional physical and/or psychological stress • Symptoms are severe but they subside within hours or days include – sudden changes in some circumstances (accidents, rape)

2. Adjustment disorder • This follows acute stress disorder usually in hospital • It is prolonged lasting up to 6 months • It is reaction to bad news or a significant event

3. Pathological or abnormal grief • This is a type of adjustment disorder • There is excessive and prolonged grief or denial of the bereavement • Repeated dreams of a dead person • Patients have anger at doctors or even the person who died him/ herself.

4. Post traumatic stress disorder This is delayed or prolonged response to stressful situation e. g: Sexual abuse War, Road Traffic Accident Human disaster

Clinical features 1. Flashbacks: relieving the event 2. Insomnia 3. Avoidance of activities – avoid similar circumstances 4. Hyper-vigilant and hyper-arousal

Treatment: CBT

Obsessive Compulsive Disorder

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They are repetitive and intrusive (interfere with personal life and activities) Common examples: 1. Checking doors locked all the time expectedly 2. Walking back and forth again and again 3. Cleaning the toilet repeatedly 4. Washing hands excessively Treatment: 1. Cognitive Behavior therapy 2. Anxiolytics – Benzodiazepine NB: Benzodiazepines: They are used for alcohol withdrawal Cause respiratory depression Lorazepam is short acting Diazepam & Chlordiazepoxide is long acting

NB: Treatment of anxiety or alcohol withdrawal use long -acting benzodiazepine.

ALCOHOL ABUSE 1. Alcohol withdrawal: • Delirium tremens • Agitation • Aggression • Tremor (Usually these symptoms appears in a patient admitted for an operation & 2-3 days after operation or hospitalization due to any other medical reason) • Confusion, Tachycardia, Hypotension • Visual hallucinations are very common in alcohol withdrawal and they are very suggestive of alcohol abuse. E.g. insects crawling in beds, tactile hallucinations.

Management of alcohol withdrawal -detoxification program use Long acting benzodiazepines 1st choice: Chlordiazepoxide 2nd choice: Diazepam

2. Wernicke’s encephalopathy • Headache • Confusion • Flapping tremor, ataxia • Opthalmoplegia.

Management: IV high potent vitamins, IV Thiamine (Vitamin B1) followed by IM thiamine

General Management of alcohol abuse: 1. Detoxification program: This is during withdrawal period use long acting benzodiazepine e.g. chlordiazepoxide Maintenance of abstinence: 1. Acamprosate: Decreases craving, decreases relapse 2. Disulfiram: Causes unpleasant symptoms if alcohol is consumed 3. Naltrexone: Not licensed in the UK for this purpose (but decreases craving and and relapses)

DRUG ABUSE

1. Opiate e. g heroin/morphine/methadone Detoxification ( during withdrawal)= use methadone Symptoms of withdrawal • Flu like symptoms • Muscle cramps • Running nose • Occurs 7-10 after stopping use of Opiates • Agitation, restlessness • Diarrhea, abdominal pain • Yawning & sweating, difficulty to sleep

Maintainance use methadone as well.

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Opiate overdose is treated with naloxone, usually there is decreased respiratory rate less than 12 and also pin point pupils or IV marks/ puncture marks on arms or legs. NB: Cocaine is not an opiate its an amphetamine analogue.

HALLUCINOGENIC DRUGS LSD-LYSERGIC ACID DIETHYLAMIDE • Causes distortion of sensory perception and visual hallucination e.g. an orange tie of the teacher is speaking to me.

COCAINE: • Usually sniffed • Dilatation of pupils • Tachycardia • Hypertension • Causes nasal perforation leading to the whistling in the nose. • Overdose can lead to Sub-arachnoid hemorrhage, myocardial ischemia and acute MI.

Withdrawal symptoms of cocaine: Tremor Depression Muscle pain

Investigation: Creatinine phosphokinase is elevated.

SCHIZOPHRENIA Symptoms: The 3 main symptoms are: 1. Hallucinations 2. Delusion 3. Thought disorder • Thought Insertion • Thought With-drawl • Thought Broadcasting • Thought Blocking • Passivity Phenomenon e.g. there is a device in the brain trying to control patient. • Blunt Effect • Incongruence Mood • No Insight

Management: Anti psychotics - Can be classified into typical and atypical Typical Eg. Haloperidol or Chlorpromazine Side effects: Neuroleptic syndrome, fever, hypothermia, tachycardia, fluctuating consciousness, increased WCC, abnormal LFT, hyperprolactinaemia Atypical Olanzapine, risperidone, clozapine, quetiapine, amisulpiride

SIDE EFFECT OF TYPICAL ANTI-PSYCHOTIC: Dopamine receptor blockage (Haloperidol and chlorpromazine) Extra-pyramidal side effect: • Parkinsonism: Brady-kinesia, tremor & rigidity • Hyper-prolactinaemia causing Galactorrhoea, Amenorrhea, Infertility, Oligomenorrhoea.

If Extra-pyramidal side effects please switch to Quetiapine.

SIDE EFFECTS OF ATYPICAL ANTI-PSYCHOTICS 1. Clozapine causes Agranulocytosis 2. Risperidone & Olanzapine can cause extra-pyramidal side effect and hyperprolactinaemia in higher doses. 3. All atypical anti-psychotic can cause sexual dysfunction e.g erectile dysfunction, low libido, low arousal, anorgasmia, sexual dysfunction, weight gain.

EATING DISORDERS Anorexia nervosa Commonly young female Mobid fear of being fat & distorted body shape Weight loss Amenorrhea BMI 2/week or (night symptoms) or if getting exacerbation move to next step. Step 2: Add regular Inhaled Steroid: Therefore at this stage child will be taking salbutamol as required and inhaled steroid e.g. beclomethasone 200 micrograms, if not helping go to 800 micrograms, if still not resolving then go to step 3. Step 3: Check diagnosis, check technique (use the spacer with a mask). Add 1 dose monteleukast (leucotriene antagonist) in the evening. If 2-5 years, add leukotriene antagonist (e. g. monteleukast), formeterol. If 5 years add Long acting – agonist e.g. salmeterol. At this stage if not getting any benefit from long acting beta-agonist them discontinue it. But if it has added some benefit then continue it. Step 4: Increased inhaled steroid up to maximum dose (e.g. Beclomethasone 800 μg --- 2000 μg). If child develops oral candida reduce the dose. At this stage also consider leukotriene antagonist if not already used or modified long acting beta agonist or aminophylline Step 5: Add prednisolone – oral

A. Unstable patient = Acute exacerbation of asthma a. Mild to moderate asthma (able to talk, Pulse < 125, PEFR > 35% of the predicted value. Oxygen > 92%.

Treatment: 1. Oxygen 2. Nebulised salbutamol 5mg every 15-30 minutes or terbutaline 3. Prednisolone

a. Severe asthma (can not speak in complete sentences in one breath or child too breathless to speak, PEFR 35%-50%, Oxygen saturation < 92%)

Treatment:

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1. Oxygen 2. Nebulised Salbutamol 5mg every 15-30 minutes ± IV salbutamol 3. Oral Prednisolone 40-50 mg or hydrocortisone 100 mg IV 4. MgSO4 5. Aminophylline after talking to ITU

a. Life threatening asthma: (Silent chest, cyanosis, hypotension, bradycardia, agitation, reduced consciousness, saturations < 92%)

1. Oxygen 2. Nebulised Salbutamol ± IV salbutamol 3. Prednisolone or hydrocortisone 4. MgSO4 5. Aminophylline

PREVENTION OF ASTHMA

1. Stop smoking 2. Avoid allergens (pets, dust) 3. Use sodium cromoglycate for exercise induced asthma or pre-exercise bronchodilator. If you have both options in the question choose sodium cromoglycate. 4. Avoid infection

PULMONARY EMBOLISM

• Usually young female with risk factor e.g. history of long flight or on combined contraception. • Sudden shortness of Breath, sudden chest pain. • Haemoptysis • Shortness of breath

RISK FACTORS OF PE: Malignancy, pregnancy, post operative especially hip operation and hysterectomy, combined oral contraception pills, long flight

Management of Pulmonary embolism

You need wells score.

Well's score

1. Entire leg swelling -------------------- +1 2. Calf swelling more than 3 cm------- +1 3. Active malignancy-------------------- +1 4. Immobilization more than 3 days---- +1 5. Pitting edema------------------------- +1 6. Collateral superficial veins----------- +1 7. Calf circumference more than 3 cm compared to other leg--- +1 8. Other diagnosis likely----------------- -2

Low probability=0 or less points Intermediate probability 1-2 point High probability 3 or more

Management:

1. Low probability --- do D-dimer first If D-dimer negative then PE has been ruled out If D-dimer positive ---> start low molecular weight heparin ---> investigate with V/Q scan ---> if confirmed continue treatment and add warfarin. If V/Q scan negative stop the low molecular weight heparin.

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2. If intermediate or probability ---> start treatment with low molecular weight heparin ---> investigate with V/Q scan if confirmed continue treatment with low molecular weight heparin and add warfarin, if negative then stop the treatment. If confirmed PE then continue both low molecular weight heparing and warfarin and stop heparin when INR reaches 2. You then continue warfarin maintaining INR 2-3. NB: In pregnancy, you use low molecular weight heparin, as warfarin is teratogenic.

Investigations in Pulmonary embolism

1. V/Q scan this is the most appropriate investigation as it expose patients to less radiation but it can only be done if CXR is normal. So if the question says CXR is normal then definitely choose V/Q scan 2. Pulmonary angiogram is the most definitive investigation and the gold standards. 3. CTPA is better than V/Q and if chest X-ray is abnormal it is always preferred. 4. D-dimer choose only if there is low probability of PE, do not choose if intermediate or high risk. Also if patient is post-operative D-dimer is not used.

NB: Maintain INR between 2-3.

TENSION PNEUMOTHORAX

As discussed earlier develops in young tall, thin men. Please see above under the section of examination.

Investigation is Chest x-ray

Treatment: Wide bore needle or cannula in the intercostal space. This is also called needle decompression. If none of the above are in the options, then you can choose chest drain.

CYSTIC FIBROSIS

• This is congenital disease affecting new born babies. it is an autosomal recessive condition and there is 1:4 or 25% chance that the other next child will be affected.

• It is chloride channel defect • As a baby there is history of recurrent chest infection, meconium ileus, failure to thrive. • Usually at the age between 18-30 the patients develop bronchiectasis as a complication. Therefore watch for the age of the patient.

Investigation: sweat test.

Treatment is symptomatic: physiotherapy, antibiotics for infection.

COPD - Chronic Obstructive Pulmonary Disease

There are 2 types COPD: emphysema type and chronic bronchitis.

This is due to smoking, therefore there is long standing history of smoking.

• Usually middle aged men 35-50. • Look at the age of the patient because long history of smoking, if elderly patient malignancy is more likely than COPD.

Investigation: Respiratory function test.

Treatment: steroid inhalers and bronchodilator Patient with COPD usually develops type 2 respiratory failure and therefore do not give 100% oxygen. Give 24% oxygen by venturi mask and do an ABG. If the amount of CO2 on 28% is increasing, then reduce to 24%.

Type 2 respiratory failure is when oxygen is less than 8 and CO2 is high (above 6).

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Type 1 respiratory failure is when oxygen is less than 8 and CO2 is normal or low.

ASPERGILLUS

Causes extrinsic allergic alveolitis -

• There is intermittent shortness of breath depending on the exposure. • It is due to exposure to aspergillus clavatus - a fungus.

Treatment: anti-fungal e.g. amphotericin

Aspergillus can cause asthma as allergic reaction due to exposure and as well it can as a complication in Asthma.

LUNG CANCER

• Usually elderly patient with chronic history of smoking • Weight loss, anorexia, anaemia • Usually this is bronchogenic carcinoma • Progressive or worsening shortness of breath, haemoptysis • Small cell lung cancer can cause SIADH with low Na and high ADH. Also, cushing’s syndrome can be cause by small cell cancer.

• Squamous cell carcinoma causes hypercalcaemia

Investigations: Bronchoscopy for bronchogenic carcinoma. CT-scan of the chest for carcinoid.

BRONCHIECTASIS This is permanent dilatation of the bronchi due to recurrent chest infection. Causes: cystic fibrosis, recurrent infection. Symptoms: chronic cough, copious purulent sputum, intermittent hemoptysis

Investigation is high resolution CT scan

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• ◦ ◦ ◦ ◦ • +44 0208 9800 039 +44 0794 0433 068

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Rheumatology PLAB 1 Notes

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Rheumatology

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SAMSONPLAB ACADEMY Bow Business Centre Bow Road 153-159 E3 2SE, London Telephone: +44(0)2089800039 Mobile: +447940433068 Email: [email protected]

RHEUMATOLOGY NOTES

Table of Contents:

1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16. 17. 18. 19. 20. 21.

Synovial Fluid Analysis Arthritis Rheumatoid Arthritis Osteoarthritis Crystal Arthropathies Spondyloarthritis Ankylosing Spondylitis Reiter’s / Reactive Arthritis Psoriatic Arthritis Viral Arthritis Septic Arthritis Autoimmune Connective Tissue Diseases Scleroderma Polymyositis and Dermatomyositis Systemic Lupus Erythromatosus Vasculitis Giant Cell arthritis Takayasu’s Arteritis PolyArteritis Nodosa (PAN) Polymyalgia Rheumatica Plasma Antibodies

1. SYNOVIAL FLUID ANALYSIS

a. Normal fluid is clear/colourless, with 500mg/kg can cause death Give activated charcoal if ingestion less than 1 hour ago and took more than >120mg/kg Check 2 hours post ingestion if patient symptomatic. If asymptomatic check at 4 hours after ingestion. Investigation: U&E, PT or INR, Blood glucose causes hypoglycaemia), ABG can cause hypokalaemia Treatment: If salicylate >500mg/kg then IV 8.4%sodium bicarbonate 225ml over 1 hour Alkalinization of urine 4. ANTIDEPRESSANT Tricyclic antidepressant (amitriptyline, dosulepin) Symptoms:

1. 2. 3. 4. 5. 6. 7. 8. 9. 10.

Tachycardia Dilated pupils Urinary retention Hyperreflexia Divergent squint Hypotension Seizures Coma Arrhythmias Prolonged QRS complex

5. Selective serotonin reuptake inhibitors (SSRIs) e.g. paroxetine, sertraline, fluoxetine, citalopram Symptoms: nausea, vomiting, tremor, serotonic syndrome

6. Selective norepinephrine reuptake inhibitors e.g. venflaxine cause same symptoms as TCA

7. Mirtazepine: vomiting, nausea and drowsiness Management: Activated charcoal if taken within 1 hour If QRS >120ms after overdose give 8.4% sodium bicarbonates 50ml serotinin syndrome may occur after taking 2 or more antidepressant e.g. TCA, SSRI or MAOI

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8. OPIOIDS EXAMPLES: codeine, morphine, dihydrocodeine, fentanyl, tramadol, methadone, pethidine. Features:

1. 2. 3. 4. 5. 6. 7.

Reduced consciousness Respiratory depression Pin point pupils Hypotension Vomiting and nausea Respiratory rate < 12 Patient may have puncture marks on the arms.

Management: Naloxone IV 0.4 - 2mg. Can also be given IM for which its effect can be more prolonged. N.B: The plasma half life of naloxone is shorter than that of most opioid, so the repeated does are often required. This is especially true with long acting opiates e.g. Morphine sulphate tablets or methadone where naloxone infusion might be needed. N.B: Opiates accumulates in the body in people with renal impairment. Therefore opiate toxicity should be suspected in all patients with unexplained type 2 respiratory failure.

1.

RECREATIONAL DRUGS

FEATURES: Stimulant drugs such as NMDA (ecstasy), amphetamines, cocaine. lysergic acid diethylamide (LSD) may cause severe agitation, tachycardia, sweating, pyrexia, dilated pupils, hypertension, arrhythmia and seizures. Severe cases results in coma, rhabdomyolysis, renal failure and subarachnoid haemorrhage, myocardial infarction, repeated seizures and death. SPECIFIC FEATURES 1. COCAINE: Coronary artery aneurysm, myocardial ischaemia and infarction and aortic dissection. Also subarachnoid

aneurysm. 2. Ecstasy: causes severe hyponatremia and water intoxication 3. Gamma hydroxybutyrate (GHB) may cause bradycardia, hypotesion, reduced consciousness and coma associated

with severe withdrawal symptoms; Management:

1. 2. 3. 4. 5.

Measure U&E, LFTs, Creatinine phosphokinase (CK) Perform ECG and monitor cardiac rhythm Hypertension settles with diazepam if still persistent then use glycerine tri-nitrate Treat cocaine induced chest pain and ECG changes with diazepam, aspirin and nitrates Amphetamine tachycardia can be treated with beta blockers

1. IRON OVERDOSE 1. Common in children of pregnant mothers, after left unsupervised and ingested mother’s iron tablets. The iron tablets are

red in colour and child may vomit reddish-brown materials. 2. Iron tablets=iron sulphate 3. Features: nausea and vomiting metabolic acidosis, stomach ulcers, liver failure, Brain damage. Brain damage and coma.

NB: stomach ulcers may cause stricture. Investigation: serum iron levels Treatment : Desferoxamine, if not improving then dialysis. 11. DIGOXIN Reduced cognition, yellow-green visual haloes, nausea, vomiting, cardiac arrhythmia. Treatment: digoxin specific anti-body fragment.

12.CYANIDE Dizziness, headache, breathlessness, shock, odour of bitter almonds. No Cyanosis

Treatment: oxygen, sodium nitrite and sodium thiosuphate, dicobalt edetate.

12. METHANOL Headache, breathlessness, photophobia, papilloedema, optic atrophy, blindness. Treatment: Gastric lavage, bicarbonate infusion, ethanol plus IV calcium.

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13. CARBON MONOXIDE Pink skin, headache, vomiting, tachycardia, tachypnoea, fits, coma and cardiac arrest Investigation: serum carbon monoxide levels, oxygen levels might be high. Managment: 100% hyperbaric oxygen, manitol for cerebral oedema.

14. ETHYLENE GLYCOL (anti-freeze) GI upset, neurological involvement, cardiorespiratory collapse, acute renal failure, Treatment: gastric lavage, bicarbonate infusion, ethanol, IV calcium.

15. ORGANOPHOSPHATE: Salivation, lacrimation, urination, diarrhea, sweating, small pupils, bradycardia, respiratory depression, muscle fasciculation Treatment: Atropine and pralidoxime

16. PARAQUAT Nausea, vomiting, diarrhea, painful oral ulcers, alveolitis, renal failure Treatment: activated charcoal. 17. LITHIUM TOXICITY Vomiting, diarrhea, coarse tremor, decreased consciousness, ataxia, increased tone, hypokalaemia Treatment: IV fluid and haemodialysis

18. PHENYTOIN TOXICITY Gum hypertrophy and cerebellar signs e.g. nystagmus, ataxia, diplopia, dizziness etc. Investigation: serum drug levels Phenytoin toxicity: renal failure and liver failure: Check U&E, INR and drug levels 19. BETA BLOCKERS AND CALCIUM CHANNEL BLOCKERS Bradycardia, hypotension and arrhythmia Treatmnet: Atropine 20. ANTI-PSYCHOTICS: Low blood pressure, ECG changes, extrapyramidal side effects: tremor and hyperprolactinaemia. 21. NSAIDs: Renal failure and heart failure. Investigation: check U&E

22. LSD: Visual hallucinations, agitation, excitement, tachycardia and dilated pupils. Hypertension and pyrexia may occur. Massive overdose may lead to coma, respiratory arrest and coagulation disturbances. Treatment is supportive.

23. ECSTASY: Euphoria, agitation, sweating, dilated pupils, ataxia, teeth grinding, headache, tachycardia, hypertension. Can lead to renal failure, liver failure, cerebral haemorrhage and coma. Treatment: 1. Consider activated charcoal if less than 1 hour since ingestion. 2. Observe for at least 4 hours 3. Monitor ECG, pulse, blood pressure and temperature

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